The researchers surveyed peer-reviewed literature published through mid-2024, searching PubMed, Google Scholar, ScienceDirect and Wiley Online Library for studies combining cannabidiol with terms covering sunscreens, antioxidants, inflammation, UV radiation and skin biology. From that search, 19 studies made the final cut: four review articles, nine in vitro experiments, three animal studies, one human clinical trial and two mixed-method investigations. The authors are candid about the limits of their approach. Because this was a narrative review rather than a systematic one, they did not apply PRISMA methodology or formal risk-of-bias assessment, and they acknowledge the search may have missed relevant work, particularly non-English publications.

The most striking findings concern CBD’s antioxidant chemistry. Structurally, the molecule shares features with vitamins E and C: phenolic hydroxyl groups attached to aromatic rings that can donate hydrogen atoms to reactive oxygen species and free radicals, interrupting the chain reactions that damage lipids, proteins and DNA. CBD is also highly lipophilic, allowing it to accumulate in cell membranes and stabilize them in a manner reminiscent of vitamin E. In rat experiments, chronic UVA and UVB exposure distorted keratinocyte membrane phospholipid metabolism, and topical CBD partially reversed those changes, downregulating harmful lysophosphatidylcholines and phospholipase A2 activity while upregulating protective phosphatidylethanolamines and phosphatidylserines. In human keratinocytes stressed with hydrogen peroxide or UVB, CBD reduced malondialdehyde and 4-hydroxynonenal, two well-established markers of lipid peroxidation, and modulated proteostasis networks governing protein folding and redox balance in ways that increased cell survival.

Beyond these direct chemical effects, CBD appears to manipulate the skin’s own antioxidant machinery. The review highlights its interaction with Nrf2, a redox-sensitive transcription factor often described as the master regulator of cytoprotective gene expression. Under normal conditions Nrf2 is held inactive by its nemesis Keap1, which tags it for destruction by the proteasome. Oxidative stress disrupts this pairing, freeing Nrf2 to enter the nucleus and switch on genes encoding superoxide dismutase, glutathione peroxidase and heme oxygenase 1. Intriguingly, keratinocyte studies suggest CBD is only a weak Nrf2 activator but a strong inhibitor of BACH1, a transcriptional repressor that works alongside Nrf2 to control heme oxygenase 1. This positions CBD as an Nrf2-independent booster of HMOX1 expression, encouraging keratinocyte differentiation and cytokeratin production, processes critical to maintaining a skin barrier that resists UV-induced DNA damage.

The anti-inflammatory story runs through a different set of molecular switches. CBD appears to be a major inhibitor of NFκB signaling, the central hub of the inflammatory response. Normally locked in the cytoplasm by its inhibitor IκB, NFκB is released when pro-inflammatory signals such as tumor necrosis factor alpha trigger IκB’s degradation, allowing the transcription factor to activate genes for cytokines, chemokines and adhesion molecules. UV irradiation drives inflammation through exactly this pathway, and in three-dimensional human keratinocyte cultures CBD counteracted it, restoring IκB levels and suppressing NFκB. CBD also dampened the NLRP3 inflammasome and the pro-inflammatory protein PGAM5, while full-spectrum CBD extract showed high-affinity inhibition of NLRP3 and TGF-β1 responses. In human skin fibroblasts, CBD elevated PPARγ, a nuclear receptor that represses inflammatory pathways, and in an acne study it significantly suppressed TNF-α, IL-1β and IL-6 in human sebocytes.

The endocannabinoid system adds yet another layer. CB2 receptors, found in immune and peripheral tissues including skin, can restrain pro-inflammatory cytokine release, and CBD’s modulation of CB2, along with its desensitization of TRPV1 channels activated by oxidative stress and its activation of adenosine A2A receptors, may collectively calm overactive immune responses in UV-damaged skin. One study of patients with psoriasis, atopic dermatitis and scarring found that a CBD-enriched ointment improved disease severity, quality of life, skin hydration and elasticity with no adverse effects. The review also flags a fascinating effect on melanocytes: CBD can activate p38 and p42/44 MAPK signaling and independently upregulate MITF, tyrosinase and related proteins, enhancing melanogenesis, the production of the pigment that naturally scatters and absorbs UV radiation. This raises potential applications for hypopigmented disorders and hints at melanin-mediated photoprotection.

But here is where the enthusiasm must be tempered, and the review is refreshingly blunt about it. Spectral analyses show that CBD absorbs UV light predominantly between roughly 220 and 280 nanometers, a range overlapping UVC, which is filtered out by the atmosphere, and only minimally touching the UVB band that sunscreens must block. In one comparative study, CBD showed the strongest cytoprotection against UVA-associated injury while cannabinol performed best against UVB, but neither CBD nor its relatives demonstrated direct photoprotective absorption at the wavelengths that matter. The authors emphasize that the observed cytoprotective effects should not be interpreted as sunscreen activity. CBD’s benefits, if real, would be indirect, working beneath the filter layer to help skin cells survive whatever radiation gets through.

Safety questions also complicate the picture. Most systematic safety data come from oral CBD, where randomized trials have identified increased risks of diarrhea, somnolence, decreased appetite and abnormal liver function tests, though the hepatic and sedation signals were concentrated in high-dose childhood epilepsy studies using drugs like clobazam and valproate. CBD is metabolized by CYP450 liver enzymes and can be a potent dose-dependent inhibitor of their activity, a concern that depends heavily on how much of a topical dose actually reaches the bloodstream. Evidence on that front is mixed: in a 17-day study of 46 healthy adults, CBD was detectable in blood after repeated use of three of five commercial topical products, though concentrations were far below those from oral or inhaled use and no cognitive or physiological effects appeared. Topical tolerability data remain thin and formulation-dependent, with patch-testing studies showing selected CBD products were non-irritating and non-sensitizing in healthy adults, while a transdermal gel trial saw application-site dryness, pain and one case of irritant contact dermatitis.

There is one tantalizing human data point. A small pilot randomized trial of nanoparticle-encapsulated topical CBD, involving just 19 participants, found less erythema on treated skin after UVA irradiation, along with reductions in epidermal hyperplasia and cellular stress and aging markers. But the study measured no SPF and included no active sunscreen comparator, so it cannot speak to whether CBD would add anything to a real product. The review also raises a subtle photochemical concern: when CBD oxidizes, it can form the cannabinoid quinone HU-331, which absorbs UV near 270 and 409 nanometers and has shown topoisomerase-II inhibition and endothelial-cell apoptosis induction in non-skin experimental systems. CBD and its hydroxyquinone have also generated reactive oxygen species during mouse liver microsomal metabolism. None of this demonstrates phototoxicity in human skin, but it marks genuine toxicologic uncertainties that demand study before CBD rides around in a sun-exposed bottle.

The regulatory landscape adds a final layer of complexity. In the United States, sunscreens are regulated as over-the-counter drugs, and only zinc oxide and titanium dioxide currently meet the FDA’s Generally Recognized as Safe and Effective standard, while the 2022 Modernization of Cosmetics Regulation Act has tightened scrutiny of cosmetic ingredients, with new 2026 legislation targeting full-spectrum CBD products specifically. Any manufacturer hoping to add CBD to a sunscreen would face registration, human safety substantiation and adverse event surveillance requirements. The review’s bottom line is measured: CBD may eventually earn a role as an adjunctive, non-filter component of photoprotective skincare, but the evidence base, dominated by in vitro and rodent work with enormous variability in models and doses, is nowhere near supporting claims of sun protection. Until standardized SPF, stability, photostability and human safety testing say otherwise, your sunscreen’s active ingredients should remain the ones with proven track records.

Subject of Research: Preclinical evidence on cannabidiol's effects against ultraviolet-induced skin damage and its potential as a sunscreen additive

Article Title: Cannabidiol and ultraviolet-induced skin damage: a narrative review of preclinical evidence and translational considerations for sunscreen additive development

Article References: Papadeas, G. G., Szeto, M. D., Reed, M. J., Paul, A., Runion, T. M., Anderson, J., & Dellavalle, R. P. (2026). Cannabidiol and ultraviolet-induced skin damage: a narrative review of preclinical evidence and translational considerations for sunscreen additive development. Archives of Dermatological Research, 318(1), Article 430. https://doi.org/10.1007/s00403-026-04888-x

Image Credits: AI Generated

DOI: 10.1007/s00403-026-04888-x

Keywords: cannabidiol, CBD, sunscreen, UV radiation, photoprotection, skin cancer, antioxidant, anti-inflammatory, keratinocytes, melanocytes, Nrf2, dermatology

The study, led by Putri Kusuma Astuti and colleagues at the University of Debrecen, focused on ten adult ewes of the Hortobágyi Racka breed, five black-coated and five white-coated, all of similar age and body weight, raised together under identical conditions and feeding management. Skin samples were collected from the posterior cervical region of each animal at an abattoir in northern Hungary in May 2023, preserved rapidly in RNAlater solution, and frozen at minus seventy degrees Celsius until analysis. By contrasting two coat colors within a single breed, the researchers deliberately minimized the confounding effects of breed-level genetic structure, allowing them to home in on expression differences genuinely associated with pigmentation rather than with broader ancestry.

The team used RNA sequencing, a technique that captures a snapshot of every gene being actively transcribed in a tissue at a given moment. Total RNA was extracted from the skin samples and converted into sequencing libraries using the QuantSeq 3′ mRNA-Seq kit, which focuses on the tail ends of messenger RNA molecules. The libraries were sequenced on an Illumina NovaSeq 6000 platform, generating more than fifty-four million reads across nine animals, as one black-coated sample failed to sequence. The reads were then aligned to the domestic sheep reference genome, the ARS-UI Ramb v3.0 assembly, using the STAR alignment tool, and gene-level counts were quantified with HTSeq. Sophisticated normalization and statistical modeling in the limma and edgeR frameworks, including the voom transformation that accounts for the peculiar mean-variance behavior of count data, allowed the researchers to identify genes whose expression differed significantly between the two color groups.

The results were strikingly one-sided. Of the 108 differentially expressed genes identified using a threshold of fold change greater than 1.5 and p less than 0.05, fully 83 were upregulated in the black-coated sheep, while only 25 were downregulated. The upregulated set was dominated by a tightly coordinated pigmentation network: melanogenesis enzymes such as TYR, TYRP1, and DCT; melanosome structural proteins including PMEL, MLANA, GPNMB, and TRPM1; melanosome transport genes like OCA2, SLC45A2, SLC24A5, and SLC24A4; and upstream melanocyte regulators including PAX3, IRF4, and RAB32. Nine of these genes, among them TYRP1, PMEL, TRPM1, MLANA, SLC24A4, SLC45A2, DCT, OCA2, and DDC, remained significant even after the most stringent multiple-testing correction. In other words, the skin of black Racka sheep is not merely darker; it is running an entire pigment-production program at far higher intensity.

Yet the story did not end with pigment. Functional enrichment analysis using Gene Ontology and KEGG pathway databases revealed that the differentially expressed genes clustered into pathways extending well beyond melanogenesis. The upregulated genes were significantly enriched in tyrosine metabolism, melanogenesis, metabolic pathways, thermogenesis, and oxidative phosphorylation, the latter being the mitochondrial process that generates most of a cell’s ATP. Gene-term networks and protein-protein interaction analysis built from the STRING database reinforced this picture, showing a coherent melanogenesis module centered on the TYR-DCT-MLANA axis, but also revealing separate modules devoted to mitochondrial and redox metabolism, involving genes such as NDUFS2, SLC25A4, QDPR, and AKR1B1, and to cell cycle and proteostasis signaling. Enriched molecular functions included calcium channel activity and calcium-potassium-sodium antiporter activity, reflecting the fact that melanin production inside melanosomes is tightly regulated by organellar ion homeostasis.

Why should coat color be entangled with cellular energy metabolism and stress biology? The authors point to a growing body of evidence that melanin synthesis is a biochemically demanding and redox-active process. Eumelanin, the pigment responsible for dark coloration, is a powerful antioxidant and an effective blocker of ultraviolet radiation, but producing it consumes cellular resources and can generate reactive oxygen species along the way. Pheomelanin, which produces lighter colors, is even more antioxidant-intensive, drawing on the cell’s stores of glutathione and cysteine. This means that the choice between dark and light pigmentation is not simply cosmetic; it carries real consequences for a skin cell’s oxidative balance, energy budget, and resilience under environmental stress such as intense sun and heat.

The study’s findings feed into an unresolved debate in livestock science about whether lighter or darker coats confer an advantage under a warming climate. Light-colored coats physically reflect more solar radiation and absorb less heat, which would seem advantageous in hot environments. Yet the evidence is mixed: some studies of grazing sheep in hot-arid conditions have found that black-coated animals maintained lower rectal temperatures than white-coated ones, while other research on goats under prolonged heat stress found white and mixed coats most adaptable. A recent gene-editing experiment in Holstein cattle, in which the PMEL gene was modified to dilute coat color, showed that lighter calves absorbed significantly less heat and light than their darker counterparts. The Racka data do not settle the question, but they suggest a mechanism by which dark pigmentation could carry its own compensatory benefits: the upregulation of genes like TRPM1, implicated in DNA repair and calcium signaling during heat stress, and TYRP1, reported to regulate oxidative stress and support cellular adaptation in extreme conditions.

There is also an intriguing immunological dimension. Melanocytes, the pigment-producing cells of the skin, are increasingly understood as active participants in immune signaling. They can present antigens to T lymphocytes, express immune-interaction molecules such as ICAM-1 and CD40, and release cytokines that shape inflammatory responses. Highly melanized melanocytes may suppress inflammation more effectively, partly through the immunosuppressive effects of L-DOPA and related compounds, whereas lightly pigmented skin may mount stronger cytokine-mediated immune signaling. The researchers also note that pigment regulation and the body’s stress-hormone system share biochemical machinery, notably the proopiomelanocortin molecule, which feeds into both pigmentation and cortisol synthesis. This overlap raises the possibility that coat color and stress physiology are coupled through shared hormonal pathways, a hypothesis the authors frame as speculative but testable.

The team validated their sequencing results using quantitative reverse-transcription PCR on ten selected genes spanning pigmentation, immune, and metabolic functions. Eight of the ten genes were confirmed to be significantly more highly expressed in black sheep skin, with TYRP1 showing the largest difference between the groups. The authors are careful, however, to spell out the limitations of their work. With only four black and five white animals, statistical power is modest, and the study included no direct measurements of heat tolerance, UV response, oxidative stress markers, or skin temperature. The links between pigmentation and adaptation remain, in their words, hypothesis-generating rather than causal, awaiting protein-level assays and controlled heat-challenge experiments in larger populations.

Even with those caveats, the study delivers a compelling molecular portrait of a famous breed and a provocative idea: that the color of a sheep’s fleece is the visible tip of a much larger biological iceberg. Beneath the black and white coats of the Hortobágyi Racka lie coordinated differences in ion transport, mitochondrial bioenergetics, redox buffering, and proteostasis, suggesting that pigmentation and environmental resilience may have evolved together. As climate change intensifies heat stress on livestock worldwide, understanding how coat color genes intertwine with cellular stress machinery could help breeders select animals not just for appearance, but for the hidden physiology that keeps them thriving in an increasingly hostile environment.

Subject of Research: Transcriptomic differences between black- and white-coated Hortobágyi Racka sheep skin

Article Title: Coat Color‐Associated Transcriptomic Differences of Black and White Hortobágyi Racka Sheep Using the RNA‐Seq Technique

Article References: Astuti, P. K., Bagi, Z., Bodrogi, L., & Kusza, S. (2026). Coat Color‐Associated Transcriptomic Differences of Black and White Hortobágyi Racka Sheep Using the RNA‐Seq Technique. Ecology and Evolution, 16(10), Article e74397. https://doi.org/10.1002/ece3.74397

Image Credits: AI Generated

DOI: 10.1002/ece3.74397

Keywords: Hortobágyi Racka sheep, coat color, RNA-seq, melanogenesis, transcriptomics, pigmentation, heat stress, oxidative stress, mitochondrial metabolism, TYRP1, melanocytes, livestock adaptation

Vitiligo affects an estimated one percent of the world’s population and is considered a classic model of CD8+ T cell-mediated autoimmunity. In patients with the disease, cytotoxic T cells infiltrate the epidermis and recognize antigens on melanocytes, releasing destructive enzymes and inflammatory signals that eliminate the pigment cells and leave the characteristic white patches on the skin. Current treatments, including topical anti-inflammatory agents and light-based therapies, offer incomplete and inconsistent benefit, and systemic immunosuppressants carry safety concerns that limit their long-term use. Against this backdrop, the research team led by investigators at Xijing Hospital of the Fourth Military Medical University in Xi’an asked a deceptively simple question: could a common food additive alter this destructive immune process?

Sucralose is one of the most widely consumed non-nutritive sweeteners on the planet, found in diet sodas, sugar-free snacks, medications and countless packaged foods marketed as low-sugar alternatives. While it has long been regarded as metabolically inert, recent years have produced accumulating evidence that sucralose is not invisible to the immune system. Earlier work has suggested that the sweetener can influence T cell responses in mice, and epidemiological discussions have raised questions about how high-intensity sweeteners interact with immune homeostasis. What remained unclear was whether sucralose could meaningfully modulate the specific arm of immunity that attacks self-tissue in autoimmune disease, and if so, through what molecular mechanism.

To answer that question, the researchers established a mouse model of vitiligo and administered sucralose orally, mimicking the route by which humans encounter the sweetener. The results were striking. Animals receiving sucralose showed a marked delay in skin depigmentation compared with untreated controls. When the investigators examined the lesions microscopically, they found reduced infiltration of CD8+ T cells into the epidermis and a corresponding preservation of melanocytes, the very cells that are normally lost as the disease progresses. In other words, the sweetener did not merely change laboratory measurements; it visibly slowed the destructive process that defines the disease in living animals.

The team then turned to human cells to determine whether the observation extended beyond mice. They isolated CD8+ T cells from the blood of patients with vitiligo as well as from healthy donors and exposed the cells to sucralose in vitro. Across both groups, the sweetener significantly downregulated the expression of two central mediators of T cell cytotoxicity: interferon-gamma, a potent inflammatory cytokine, and granzyme B, the serine protease that T cells deploy to punch lethal holes in target cells. By suppressing these effector molecules, sucralose effectively reduced the killing capacity of activated CD8+ T cells, the same cells that in vitiligo patients hunt down and destroy melanocytes.

Having established that sucralose dampens T cell effector function, the researchers sought the molecular switch responsible. Using transcriptomic analysis, a technique that profiles the activity of thousands of genes simultaneously, they screened for genes that responded to sucralose exposure in CD8+ T cells. One candidate stood out: interleukin-20 receptor subunit beta, or IL-20RB, a component of a cell-surface receptor belonging to the interleukin-20 cytokine family. In sucralose-treated T cells, IL-20RB was significantly upregulated, suggesting that the sweetener’s effects might be routed through this receptor subunit rather than through a diffuse, nonspecific mechanism.

To test whether IL-20RB was merely a bystander or a genuine mediator of the immunosuppressive effect, the team performed a series of functional validation experiments. When they knocked down IL-20RB expression in CD8+ T cells, the ability of sucralose to inhibit T cell activation was substantially weakened, indicating that the receptor subunit is required for the sweetener’s action. Conversely, when they forced overexpression of IL-20RB in the absence of sucralose, the cells displayed the same immunoregulatory profile that sucralose normally induces. This gain-of-function and loss-of-function symmetry provides strong evidence that IL-20RB sits on the causal pathway: sucralose acts by upregulating IL-20RB, and IL-20RB in turn restrains the activation and effector function of cytotoxic T cells.

The implications of this pathway extend beyond vitiligo. CD8+ T cells are central players in a spectrum of autoimmune diseases, including type 1 diabetes, autoimmune thyroid disease and certain forms of inflammatory skin disease, and they also shape the immune response to tumors, where their cytotoxic function is generally desirable. Any dietary compound that reliably modulates CD8+ T cell activity therefore warrants careful scrutiny in both directions. The authors frame their findings as evidence for a novel diet-responsive immune regulatory pathway and suggest that sucralose, or agents that mimic its effect on IL-20RB, could inspire new dietary or pharmacological strategies for immunomodulation in T cell-mediated autoimmunity.

At the same time, the researchers are explicit about the limits of the current evidence. The study is exploratory, and the authors emphasize that the findings warrant further investigation under physiologically relevant conditions before any conclusions can be drawn about consuming sucralose as a therapeutic strategy. Laboratory models and isolated cells do not capture the full complexity of human metabolism, long-term exposure, dose dependence, or the gut microbiome’s role in processing the sweetener. Notably, the study also assessed a broad panel of safety-related biochemical parameters, including liver enzymes such as alanine aminotransferase and aspartate aminotransferase, bilirubin, alkaline phosphatase, kidney markers including blood urea nitrogen and creatinine, and lipid and glucose measures, reflecting the team’s attention to whether sucralose administration produced systemic toxicity in their model.

For now, the study stands as a provocative example of how everyday food chemistry can intersect with immunology in unexpected ways. It adds sucralose to a growing list of dietary components, from dietary fiber metabolites to salt, whose effects on T cell behavior are far more specific than once assumed. The identification of IL-20RB as a sucralose-responsive gene gives researchers a concrete molecular target to interrogate, one that could potentially be exploited to design safer immunomodulatory interventions for vitiligo and related conditions. Whether the sweetener’s immunosuppressive pathway can be harnessed safely and effectively in patients remains an open question, but the work demonstrates that the boundary between nutrition and immunology is thinner than many imagined, and that the contents of a diet soda may carry immunological consequences that science is only beginning to map.

Subject of Research: Immunomodulatory effects of the artificial sweetener sucralose on CD8+ T cell-mediated autoimmunity in vitiligo

Article Title: Sucralose attenuates CD8+ T cell-mediated autoimmunity via IL-20RB upregulation: implications for dietary immunomodulation in vitiligo

Article References: Xu, Y., Yin, H., Wang, M., Zhu, Q., Wang, X., Guo, W., He, L., Chen, J., Li, S., & Li, C. (2026). Sucralose attenuates CD8+ T cell-mediated autoimmunity via IL-20RB upregulation: implications for dietary immunomodulation in vitiligo. Journal of Translational Medicine. https://doi.org/10.1186/s12967-026-09064-3

Image Credits: AI Generated

DOI: 10.1186/s12967-026-09064-3

Keywords: sucralose, vitiligo, autoimmunity, CD8+ T cells, IL-20RB, interferon-gamma, granzyme B, dietary immunomodulation, artificial sweeteners, melanocytes, Journal of Translational Medicine, T cell activation

The study’s design reflects a growing trend in dermatology research: the use of large national claims and health records databases to follow thousands of patients over time. Retrospective cohort studies of this kind identify individuals who already carry a diagnosis of interest, in this case vitiligo, and then track whether they develop an outcome of interest, here autoimmune thyroid disorders, over subsequent years. By comparing the incidence of thyroid disease in the vitiligo cohort against a matched comparison group, the researchers can estimate whether vitiligo patients genuinely face an elevated risk, or whether earlier reports were skewed by small sample sizes, referral bias, or the particular characteristics of single-clinic populations.

The biological rationale for a connection between vitiligo and thyroid autoimmunity is compelling. Both conditions involve the immune system losing tolerance to the body’s own tissues. In vitiligo, CD8-positive cytotoxic T cells attack melanocytes in the skin, driven in part by inflammatory signaling molecules such as interferon-gamma and the chemokine CXCL10, which recruits destructive immune cells to the skin. In autoimmune thyroid disease, which includes Hashimoto’s thyroiditis and Graves’ disease, the immune system targets thyroid proteins such as thyroglobulin and thyroid peroxidase, or stimulates the thyroid-stimulating hormone receptor. Shared genetic susceptibility loci, particularly within the human leukocyte antigen region on chromosome 6, which governs how immune cells present self-antigens, are thought to predispose individuals to both diseases simultaneously.

Earlier evidence has consistently pointed in the same direction. A 2023 systematic review and meta-analysis published in the Journal of Investigative Dermatology, led by Jung Min Bae and colleagues, aggregated comorbidity data across numerous studies and found that patients with vitiligo carry a significantly increased burden of autoimmune and thyroid-related conditions. A separate meta-analysis by Fan, Yang, and Huang published in the European Journal of Dermatology in 2018 similarly concluded that vitiligo and thyroid disease co-occur far more often than chance would predict. Population-level work has also supported the link: a nationwide study in Korea using health insurance data found that patients with vitiligo were more likely to be diagnosed with overt thyroid diseases than matched controls, suggesting the association holds at the scale of entire health systems rather than only in specialized clinics.

Yet the clinical literature has not been entirely unanimous. A study published in the British Journal of Dermatology in 2012 by Kroon and colleagues examined routine thyroid screening in asymptomatic vitiligo patients and reported a low yield of clinically significant abnormalities, raising questions about whether universal screening of every vitiligo patient is cost-effective or medically necessary. That tension, between epidemiological evidence of increased risk and the practical question of who should be tested and how often, is precisely the kind of question that large database studies are positioned to answer. By capturing diagnoses across many centers and many years, rather than relying on single-institution screening programs, a national database approach can estimate the real-world incidence of thyroid disease in the vitiligo population with far greater statistical power.

The new study by Islam and colleagues, which included co-authors Andrew J. Malek, Kazi N. Islam, Collins T. Langley, and Christopher J. Haas, was structured as a research letter, a concise format that presents key findings from large datasets. The multi-center retrospective design means the investigators did not intervene in care or recruit patients prospectively; instead, they mined existing records to assemble their cohorts and compare outcomes. The authors report that vitiligo patients showed an increased risk of autoimmune thyroid disorders relative to patients without vitiligo, consistent with the direction of effect reported in prior meta-analyses and nationwide studies. The authors declare no competing interests, and because the work involved analysis of de-identified database records, institutional review board approval and patient consent were not applicable under the study’s ethics declarations.

Why should this matter to the millions of people worldwide who live with vitiligo? The prevalence of vitiligo is estimated at roughly one percent or less in most populations, but because the condition is visible and often socially stigmatizing, patients frequently interact with dermatologists over many years. If those patients also face a meaningfully elevated risk of thyroid autoimmunity, then the skin clinic becomes a natural point of contact for preventive care. Autoimmune thyroid disease often develops insidiously: hypothyroidism from Hashimoto’s thyroiditis can cause fatigue, weight gain, cold intolerance, and depression, while Graves’ disease can produce hyperthyroid symptoms such as palpitations, anxiety, heat intolerance, and weight loss. Both are readily detectable with simple blood tests measuring thyroid-stimulating hormone and, where indicated, thyroid antibodies such as anti-thyroid peroxidase.

The mechanistic overlap between the two diseases also makes vitiligo a valuable window into autoimmunity more broadly. Researchers studying why the immune system turns on melanocytes have identified shared pathways with other organ-specific autoimmune conditions, including the roles of specific HLA haplotypes, regulatory T cell dysfunction, and cytokine networks that amplify tissue-specific inflammation. Notably, some of the same immunological circuits implicated in vitiligo and thyroid disease also appear in conditions such as type 1 diabetes, alopecia areata, and systemic lupus erythematosus. Drugs that block these pathways, for example antibodies targeting the chemokine receptor CXCR3 or inhibitors of interferon signaling, are being explored as treatments for vitiligo, and understanding the full spectrum of autoimmune comorbidity helps researchers anticipate how such therapies might influence or be influenced by coexisting thyroid disease.

For clinicians, the practical takeaway from the accumulating evidence is a matter of calibration rather than revolution. Guidelines and expert commentary have increasingly suggested that patients with vitiligo, particularly those with additional risk factors such as a family history of thyroid disease, female sex, adult onset, or non-segmental patterns of pigment loss, warrant at least baseline thyroid function testing, with periodic reassessment depending on symptoms and initial results. The new database study strengthens the epidemiological foundation for that approach, even as it leaves open the question of the optimal screening interval. It also underscores the importance of educating patients: a person being treated for pigment loss may not connect symptoms like persistent fatigue or a racing heartbeat with their skin condition, and may not know that the two are immunologically linked.

As with any retrospective database study, some caveats apply. Administrative records depend on diagnostic coding, which can misclassify or miss conditions, and patients who see dermatologists regularly may simply be more likely to have thyroid disease detected incidentally, a form of surveillance bias that careful matching and study design attempt to minimize. The research letter format also means the authors present their core findings concisely, and readers will look to the full methods for details on how cohorts were matched and how confounders such as age, sex, and other autoimmune diseases were handled. Even so, the study joins a growing and now quite consistent body of evidence that vitiligo is a systemic autoimmune condition with clinically meaningful associations beyond the skin. For a disease once dismissed as purely cosmetic, that reframing carries real consequences for how patients are monitored, counseled, and treated across their lifetimes.

Subject of Research: The association between vitiligo and autoimmune thyroid disorders assessed through a large-scale national database cohort study

Article Title: Increased risk of autoimmune thyroid disorders in vitiligo patients: a large-scale multi-center retrospective cohort study using a national database

Article References: Islam, R. K., Malek, A. J., Islam, K. N., Langley, C. T., & Haas, C. J. (2026). Increased risk of autoimmune thyroid disorders in vitiligo patients: a large-scale multi-center retrospective cohort study using a national database. Archives of Dermatological Research, 318(1), Article 456. https://doi.org/10.1007/s00403-026-04960-6

Image Credits: AI Generated

DOI: 10.1007/s00403-026-04960-6

Keywords: vitiligo, autoimmune thyroid disease, Hashimoto's thyroiditis, Graves' disease, melanocytes, autoimmunity, retrospective cohort study, national database, dermatology, thyroid screening, HLA genes, comorbidity

The review, led by Barbara Kamińska together with Aleksandra Białczyk and Rafał Czajkowski, systematically searched PubMed and Web of Science from database inception through April 16, 2025, without language or date restrictions. After screening 1,264 initially identified records, the team retained 33 original observational studies, 12 cross-sectional and 21 case-control investigations, published between 2011 and 2024. Sample sizes ranged from 30 to 896 participants. Geographically, the evidence base was heavily skewed: 26 studies came from Asia, five from Europe, and only two from the Americas, a concentration the authors flag as a potential limitation for generalizability.

The headline numbers are striking. Among the 17 studies that reported the prevalence of metabolic syndrome, a cluster of risk factors including central obesity, elevated blood pressure, impaired glucose metabolism, and dyslipidemia, 505 of 1,473 patients with vitiligo, or 34.3 percent, met diagnostic criteria, most commonly those set by the NCEP ATP III guidelines. In control groups, by contrast, only 240 of 1,289 participants, or 18.6 percent, qualified. Thirteen of the 15 studies providing comparative data found higher rates of metabolic syndrome in the vitiligo groups. Individual study estimates varied widely, from 6.7 percent to 50.7 percent, a spread the authors attribute to differing diagnostic thresholds, patient selection, and regional metabolic backgrounds.

Insulin resistance, the reduced ability of cells to respond to normal circulating levels of insulin, told a similar story. The most widely used proxy, the Homeostasis Model Assessment of Insulin Resistance, or HOMA-IR, is calculated as fasting plasma insulin multiplied by fasting plasma glucose and divided by 22.5. Across seven studies that applied HOMA-IR cut-off values, insulin resistance was identified in 279 of 494 patients with vitiligo, or 56.5 percent, versus 125 of 380 controls, or 32.9 percent. In every one of the six comparative studies, the prevalence was higher in the vitiligo group. Reported rates among patients ranged from 26.7 percent to 88.7 percent, and one study that excluded people with diabetes still found insulin resistance in 63 percent of its vitiligo cohort.

Supporting biochemical data reinforced the pattern. Across ten studies, mean fasting glucose in vitiligo patients averaged 95.66 mg/dL compared with 78.5 mg/dL in controls, while mean fasting insulin averaged 12.96 µIU/mL against 9.01 µIU/mL in control participants. Lipid abnormalities also appeared repeatedly: decreased HDL cholesterol, elevated LDL-to-HDL ratios, and increased triglycerides were frequently documented. Some studies reported higher insulin and C-peptide levels even in non-diabetic patients, hinting at early metabolic dysregulation, although at least one investigation observed a more favorable lipid profile in vitiligo patients, underscoring the inconsistency across the literature.

Whether these metabolic changes track with the severity or duration of vitiligo remains contested. Several studies found that active disease, greater body surface area involvement, and higher scores on the Vitiligo Area Scoring Index or the Vitiligo Disease Activity score predicted metabolic syndrome, insulin resistance, or elevated levels of inflammatory and metabolic biomarkers such as FABP4, VAP-1, and YKL-40. Disease severity has also been identified as an independent predictor of metabolic syndrome and subclinical atherosclerosis, and one study reported a strong correlation between serum homocysteine and VASI scores. Yet other investigations found no relationship between severity measures and metabolic indicators, and the evidence on disease duration is similarly divided, with some studies linking longer duration to metabolic risk and one even finding metabolic syndrome more common in patients with shorter disease duration, possibly reflecting higher disease activity early in its course.

The biological plausibility of a skin-metabolism connection rests on shared mechanisms of oxidative stress, chronic inflammation, and mitochondrial dysfunction. Reactive oxygen species are believed to sensitize melanocytes to immune-mediated destruction in vitiligo, and the same redox imbalance promotes serine phosphorylation of insulin receptors, disrupting insulin signaling and impairing glucose metabolism. Proinflammatory cytokines, including interleukin-1, interleukin-6, and tumor necrosis factor-alpha, are elevated in both conditions and further amplify the pro-oxidative state. Melanocytes resident in adipose tissue normally exert anti-inflammatory effects and reduce reactive oxygen species; their loss may contribute to increased oxidative stress and lipid peroxidation throughout the body.

Recent work has pushed this mechanistic story to the cellular level. Keratinocytes, melanocytes, and fibroblasts all express functional insulin and insulin-like growth factor 1 receptors, implicating insulin-dependent signaling in skin homeostasis. Experimental data show that IGF-1 can reduce oxidative damage and inflammatory cytokine production in skin models, while clinical studies report decreased serum IGF-1 levels in patients with vitiligo. Most provocatively, a 2025 study by Caputo and colleagues provided the first direct evidence of insulin resistance in keratinocytes and melanocytes derived from vitiligo patients, demonstrating impaired mitochondrial ATP production and altered cellular energy sensing despite normal extracellular glucose levels. This suggests that intrinsic mitochondrial dysfunction may underlie both the cutaneous and systemic metabolic features of the disease, opening potential avenues for therapies aimed at metabolic reprogramming.

The authors are careful about what the evidence can and cannot show. Because of considerable heterogeneity in study designs, diagnostic criteria for metabolic syndrome, and HOMA-IR thresholds, which ranged from greater than 1.93 to greater than 2.9 across studies, a quantitative meta-analysis was not feasible, and the findings were synthesized narratively. Most included studies were cross-sectional and focused on disease presence rather than progression, so causal relationships remain uncertain. Methodological quality was assessed with the Newcastle-Ottawa Scale by two independent reviewers, with a third resolving disagreements. The reviewers also note that most studies did not specify whether individuals with diabetes were excluded or analyzed separately, complicating interpretation of some glucose data, and that the geographic concentration of studies in Asia and the Middle East may limit how broadly the conclusions apply.

Even with those caveats, the practical message for clinicians is clear. The review argues that metabolic screening deserves consideration in patients with vitiligo, particularly those with active, extensive, or long-standing disease, much as it is now routine for patients with severe psoriasis. If future prospective, multicenter studies with standardized definitions confirm the association, and clarify whether metabolic disturbances play a causal role in vitiligo pathogenesis or progression, targeted metabolic interventions might one day improve outcomes for a disease currently treated almost exclusively as a disorder of pigmentation. For the millions of people living with vitiligo worldwide, the skin may finally be recognized as a window into the body’s deeper metabolic health.

Subject of Research: Association between vitiligo and cardiometabolic risk, specifically insulin resistance and metabolic syndrome

Article Title: Insulin resistance and metabolic syndrome in patients with vitiligo: a systematic review and narrative synthesis

Article References: Kamińska, B., Białczyk, A., & Czajkowski, R. (2026). Insulin resistance and metabolic syndrome in patients with vitiligo: a systematic review and narrative synthesis. Archives of Dermatological Research, 318(1), Article 455. https://doi.org/10.1007/s00403-026-04909-9

Image Credits: AI Generated

DOI: 10.1007/s00403-026-04909-9

Keywords: vitiligo, metabolic syndrome, insulin resistance, HOMA-IR, melanocytes, oxidative stress, autoimmune disease, cardiometabolic risk, systematic review, inflammation, IGF-1, dermatology

The researchers began with a straightforward hypothesis grounded in clinical observation. Solar lentigines are characterized by persistent basal hyperpigmentation, meaning that the deepest layer of the epidermis remains loaded with melanin long after the original sun exposure that triggered it. They proposed that a sustained stress response centered on IRE1α, a sensor protein embedded in the endoplasmic reticulum membrane, could act on both sides of the pigment equation at once. IRE1α is best known as a key initiator of the unfolded protein response, a cellular quality-control program that activates when misfolded proteins accumulate. When the stress is brief, the response is protective; when it becomes chronic, it can push cells toward senescence, a state of permanent growth arrest.

To test the idea, the team combined human tissue analysis with mechanistic experiments in cell culture. They examined paired samples of lesional and non-lesional skin from patients with solar lentigines, work approved by the Institutional Review Board of Severance Hospital, and complemented the histology with two laboratory models: MNT-1 melanocytes, the pigment-producing cells of the skin, and HaCaT keratinocytes, the cells that form the bulk of the epidermis and normally receive and degrade transferred melanosomes. Crucially, the keratinocyte model included a doxycycline-inducible system as well as constitutive IRE1α expression, allowing the researchers to switch the stress pathway on at will and observe the consequences in a controlled manner.

The tissue findings set the stage. In lesional epidermis, the investigators observed dense accumulations of stage-IV melanosomes, the fully mature, heavily pigmented organelles that melanocytes manufacture and hand off to keratinocytes. Alongside this pigment load, the stressed skin showed elevated levels of IRE1α and p16, a canonical marker of cellular senescence. This co-occurrence was the first hint that the two phenomena, aging-like growth arrest and pigment retention, might share a common driver rather than being parallel but independent consequences of sun damage.

Experiments in the cell models then dissected the mechanism in detail. When the researchers sustained IRE1α signaling, cell proliferation dropped and the senescence markers p16 and p21 rose, confirming that chronic endoplasmic reticulum stress is sufficient to push these epidermal cells into a senescent state. In the melanocytes, the consequences for pigmentation were direct and measurable: IRE1α activation increased tyrosinase activity, the rate-limiting enzymatic step of melanin synthesis, and raised total melanin content. The cells also produced more melanosomes, and those melanosomes were larger than normal, expanding the raw supply of pigment available for transfer to surrounding keratinocytes.

The second half of the dual-hit mechanism emerged from the keratinocyte experiments. Keratinocytes are not passive pigment containers; they are supposed to degrade the melanosomes they receive through lysosomal pathways, a process sometimes described as melanophagy. Under sustained IRE1α signaling, that degradation slowed markedly. The researchers quantified intracellular melanosomes and found they accumulated because they were being broken down more slowly, not because more were arriving. Probing the lysosomal system, they detected diminished LysoTracker signal, indicating reduced lysosomal acidity, along with reduced maturation of cathepsin-B, a key degradative enzyme that requires an acidic environment to become fully active. Autophagic flux, measured with a mRFP–GFP–LC3 reporter that distinguishes early autophagosomes from mature autolysosomes, was also compromised, with fewer autolysosomes forming.

Together, these results sketch a coherent pathological circuit. Chronic IRE1α signaling in melanocytes ramps up melanogenesis, flooding the epidermis with pigment, while the same stress pathway in keratinocytes weakens the lysosomal machinery responsible for clearing that pigment away. The senescent state that accompanies the stress response likely stabilizes the situation, since senescent cells persist in tissue rather than being replaced, maintaining the altered signaling environment over time. The net effect is that pigment is produced faster and cleared more slowly, exactly the combination needed to explain the dense, persistent basal hyperpigmentation that defines solar lentigines.

The study also points toward intervention. The researchers tested two agents: verapamil, a calcium channel blocker better known as a cardiovascular drug, and STF083010, a selective inhibitor of the IRE1α RNase domain, the enzymatic activity through which IRE1α transmits its stress signal. Both compounds lessened melanosome accumulation in the keratinocyte model and partially restored degradative function. While the restoration was partial, the finding is significant because it demonstrates that the pigment-retention phenotype is not irreversible and that the IRE1α–lysosome axis is a plausible therapeutic target. Existing treatments for solar lentigines, such as laser therapy and topical depigmenting agents, aim primarily at melanin production or destruction; a strategy that instead restores the clearance machinery would represent a fundamentally different approach.

The broader implications extend beyond cosmetically visible age spots. The unfolded protein response has been implicated in a wide range of age-related tissue changes, and this study adds a vivid example of how a single stress sensor can couple senescence to a tissue-specific functional outcome, in this case pigmentation. The work also highlights melanophagy as an underappreciated control point in skin color biology. Most research on hyperpigmentation has focused on melanocytes and their synthetic output, but the fate of melanosomes after transfer is equally decisive, and lysosomal acidification and cathepsin maturation emerge from this study as actionable levers. If the findings hold up in further clinical studies, modulating IRE1α activity or supporting lysosomal function could inform the development of treatments not only for solar lentigines but potentially for other disorders of pigment retention.

The research, funded by the National Research Foundation of Korea, Yonsei University College of Medicine and the Korea Health Technology R&D Project, was published as an open-access article and is citable under DOI 10.1007/s00018-026-06389-6. Its central message is elegant in its economy: one stress pathway, acting chronically, produces pigment faster and disposes of it more slowly, while locking the affected cells into senescence. For the millions of people who develop these stubborn brown patches, the study offers something more concrete than a new description of the problem, namely a defined molecular axis that can, at least in laboratory models, be pharmacologically nudged back toward balance. Translating that laboratory result into safe and effective clinical therapy will require further work, but the identification of the IRE1α and lysosome axis as a coupled driver of senescence and pigment retention gives the field a clear and testable direction.

Subject of Research: Chronic endoplasmic reticulum stress linking cellular senescence to persistent skin hyperpigmentation in solar lentigines

Article Title: Chronic ER stress couples cellular senescence with pigment retention

Article References: Hwang, S., Kim, J. Y., Lee, E. J., Oh, D., Bae, Y. J., Kwon, I. J., Park, S., Seo, H. R., Alqahtani, J., Lee, J., & Oh, S. H. (2026). Chronic ER stress couples cellular senescence with pigment retention. Cellular and Molecular Life Sciences. https://doi.org/10.1007/s00018-026-06389-6

Image Credits: AI Generated

DOI: 10.1007/s00018-026-06389-6

Keywords: solar lentigo, IRE1α, unfolded protein response, ER stress, cellular senescence, melanophagy, melanogenesis, lysosomal acidification, keratinocytes, melanocytes, p16, skin aging

The research team, led by Andrés Caicedo of Universidad San Francisco de Quito in Ecuador together with a broad international consortium, set out to answer a deceptively simple question: do skin cells share mitochondria with one another under normal conditions, and does that sharing change when the skin is under assault from sunlight? Horizontal mitochondrial transfer, or HMT, is an emerging form of intercellular communication that has been documented in other tissues, where stressed or damaged cells can receive functioning mitochondria from healthier neighbors, restoring their energy supply and improving their survival. But whether the cells of the epidermis and dermis engage in this exchange, and how it might relate to regenerative strategies built around mitochondria, remained poorly understood.

To find out, the investigators used a coculture system in which donor cells were labeled with MitoTracker Red, a fluorescent dye that stains active mitochondria, while recipient cells carried a green tag. When red-labeled organelles appeared inside green recipient cells, transfer had occurred, and fluorescence microscopy allowed the team to quantify how often it happened. The experiments were run in two configurations: direct two-dimensional coculture, in which donor and recipient cells physically touch, and transwell systems, in which a porous membrane separates the two populations while still allowing soluble factors to diffuse through. This design allowed the researchers to distinguish contact-dependent transfer from contact-independent mechanisms.

The results were unambiguous. Under basal conditions, transfer from melanocytes to keratinocytes was already the dominant route of exchange, and when the cells were exposed to ultraviolet radiation the transfer rate climbed dramatically, reaching approximately 39 percent of recipient keratinocytes in direct coculture. In transwell assays, where cells could not touch, the same donor–recipient pair transferred at less than 9 percent, indicating that the exchange relies overwhelmingly on direct cell-to-cell contact rather than on mitochondria or mitochondrial fragments drifting through the culture medium. Every other donor–recipient combination among the three skin cell types remained below 4 percent, and some pairs—melanocyte to melanocyte, keratinocyte to keratinocyte, melanocyte to fibroblast, and keratinocyte to melanocyte—showed no detectable transfer at all. Fibroblasts, notably, took up very few mitochondria from any source, whether from their own kind or from other skin cells, even after ultraviolet exposure.

That last observation may carry the most physiological weight. Keratinocytes, which form the outermost barrier of the skin and absorb much of the ultraviolet dose, appear to receive mitochondrial help precisely when they need it most, drawing functional organelles from melanocytes, the pigment-producing cells that sit alongside them in the basal epidermis. Fibroblasts, by contrast, live deeper in the dermis where ultraviolet penetration is weaker, but their apparent inability to import mitochondria suggests they may lack a stress-adaptation pathway available to their epidermal neighbors. The authors propose that this contact-dependent, cell-type-specific exchange represents a built-in resilience mechanism for the skin’s protective barrier, one that has gone unnoticed because it only operates at meaningful levels between particular cell pairs and under particular kinds of stress.

Having established that skin cells naturally share mitochondria, the team turned to the therapeutic question: can this process be exploited deliberately? The answer came in two stages. The first was artificial mitochondrial transfer, or AMT, performed in the laboratory. The researchers isolated mitochondria from three sources—human dermal fibroblasts, human Wharton’s jelly mesenchymal stem/stromal cells (WJ-MSCs) derived from umbilical cord tissue, and mouse bone marrow mesenchymal stem cells (BM-MSCs)—and delivered them to recipient fibroblasts. Before use, the isolated organelles were rigorously quality-controlled: scanning electron microscopy confirmed their structural integrity, tetramethylrhodamine methyl ester staining demonstrated that they retained an active membrane potential, and oxygraph measurements confirmed that they consumed oxygen and respired on substrates such as glutamate, pyruvate, and malate. These were not cellular debris but functioning bioenergetic machines.

When these stem-cell-derived mitochondria were delivered to fibroblasts, two clinically relevant effects emerged. First, WJ-MSC-derived mitochondria reduced the burst of reactive oxygen species, or ROS, that ultraviolet radiation normally triggers in skin cells, pointing to a direct antioxidant and protective function. Second, mitochondria from both human WJ-MSCs and mouse BM-MSCs significantly increased fibroblast proliferation, though the magnitude of the effect depended on the dose of mitochondria delivered, underscoring that dosing will be a critical parameter in any future clinical protocol. Fibroblasts are the workhorses of wound repair, producing collagen and rebuilding the dermal matrix, so a cell-free treatment that simultaneously lowers oxidative damage and boosts their proliferation could be valuable for burns, chronic wounds, and radiation-injured skin.

The second stage moved from the dish to living animals. In a murine model of primary-intention wound healing, the researchers applied mitochondria isolated from mouse BM-MSCs directly to the wounds. Histological analysis showed enhanced early tissue repair, and the effects were comparable to those achieved by administering the intact stem cells themselves—a remarkable result, because it suggests that at least part of the regenerative benefit of mesenchymal stem cell therapy can be reproduced by their mitochondria alone, without the cells. This has profound implications. Live stem cell therapies face hurdles of manufacturing complexity, immune compatibility, tumorigenicity concerns, and regulatory scrutiny; mitochondria are simpler, cannot replicate on their own, and could in principle be standardized, stored, and dosed like a conventional biologic.

To confirm the findings in a species whose skin more closely resembles our own, the team repeated the experiment in pigs, applying mitochondria derived from human Wharton’s jelly MSCs to primary-intention wounds. The outcomes were measured with a wound healing index, histological assessment of tissue organization, and spatial quantification of Ki67, a protein marker of actively dividing cells. Treated wounds showed a higher wound healing index, improved organization of collagen-containing tissue, and increased Ki67 positivity in both the epidermal and dermal regions directly involved in repair. In other words, the transplanted mitochondria appeared to wake up the local proliferative response on both sides of the skin’s architecture, driving new cell generation precisely where the healing front was advancing.

Taken together, the study draws a translational line between a naturally occurring behavior of skin cells and a new class of cell-free regenerative medicine. On one end, melanocytes appear to act as mitochondrial donors to keratinocytes under ultraviolet stress, a contact-dependent rescue mechanism that may help explain how skin tolerates lifelong sun exposure. On the other end, mitochondria isolated from mesenchymal stromal cells can be manufactured, applied to wounded tissue, and shown to accelerate healing across two mammalian species. The authors argue that this establishes a coherent biological rationale for mitochondria-based therapies in dermatology and wound care. Much work remains—optimal dosing, delivery vehicles, immunological considerations, and eventual human trials—but the conceptual advance is clear: the mitochondria that power our cells may one day be prescribed like medicine, harvested from stem cells and delivered to the skin to quench oxidative damage and rebuild what injury has destroyed.

Subject of Research: Horizontal mitochondrial transfer and mitochondrial transplantation for protection against ultraviolet radiation-induced damage and enhancement of skin wound healing

Article Title: Horizontal mitochondrial transfer and mitochondrial transplantation in skin: protection against UVR-induced ROS damage and enhancement of cell proliferation and wound healing

Article References: Horizontal mitochondrial transfer and mitochondrial transplantation in skin: protection against UVR-induced ROS damage and enhancement of cell proliferation and wound healing. (n.d.). https://doi.org/10.1186/s12967-026-08801-y

Image Credits: AI Generated

DOI: 10.1186/s12967-026-08801-y

Keywords: mitochondria, horizontal mitochondrial transfer, mitochondrial transplantation, skin, ultraviolet radiation, reactive oxygen species, mesenchymal stem cells, wound healing, keratinocytes, melanocytes, fibroblasts, regenerative medicine