The authors frame skin aging as a two-front battle. Intrinsic aging unfolds over time through genetic and metabolic factors, producing atrophy, dryness and fine lines in areas the sun never touches. Extrinsic aging is driven by the environment, and ultraviolet radiation dominates it, accounting for roughly 80 percent of visible signs of skin aging. UVB rays, spanning 280 to 320 nanometres, strike the epidermis and can directly damage DNA, while longer UVA wavelengths penetrate to the dermis and generate reactive oxygen species that corrode cellular machinery. The hallmark of this photoaging is solar elastosis, an abundance of pathologically altered elastic fibres that leaves chronically sun-exposed skin leathery and lax. Air pollution and smoking add further oxidative insult, but it is the interplay between external damage and internal cellular failure that the review places at the centre of the story.

That interplay plays out through four principal cell types. Fibroblasts, the workhorses of the dermis, synthesize type I and type III collagen and elastin, the structural proteins that keep skin firm and resilient. When fibroblasts senesce, they stop producing these components and instead secrete matrix metalloproteinases, enzymes that chew through the extracellular matrix. The result is dermal atrophy, reduced elasticity and wrinkling. Intriguingly, fibroblast senescence has a dual character in wound healing: in young mice, a transient wave of senescent fibroblasts secretes platelet-derived growth factor AA that drives myofibroblast differentiation and efficient wound closure, but as p21-positive senescent fibroblasts accumulate with age, proliferation stalls and repair is delayed. Senescent myofibroblasts also reduce expression of alpha-smooth muscle actin, a key contractile protein, undermining wound contraction and limiting fibrosis in ways that complicate healing in older tissue.

Macrophages add an inflammatory dimension. These immune cells normally clear debris and pathogens, with pro-inflammatory M1 macrophages dominating the early phase of wound repair and anti-inflammatory M2 macrophages steering the transition to tissue rebuilding. In aged skin, this balance tips: macrophages show reduced proliferative and phagocytic capacity, polarization shifts toward M1, and pro-inflammatory gene expression rises. The consequences for structure are concrete—fewer M2 cells mean reduced synthesis of collagen types I, V and VI, while excess M1 activity ramps up metalloproteinase-mediated collagen degradation. Keratinocytes, the dominant epidermal cell, slow their renewal with senescence, thinning the epidermis, increasing moisture loss and opening the door to pathogens such as Staphylococcus aureus. Epidermal stem cells, meanwhile, lose the proliferative vigour needed for re-epithelialization; reduced PGC-1α impairs their differentiation in aged mice, and an age-related decline in SIRT7 disrupts Nfatc1-mediated quiescence of hair follicle stem cells, contributing to the hair thinning so characteristic of aging skin.

At the molecular level, the review identifies reactive oxygen species and DNA damage as primary instigators. Excess ROS activate the transcription factors AP-1 and NF-κB through MAPK signalling, driving expression of matrix metalloproteinases that degrade collagen and elastin while simultaneously suppressing synthesis of new matrix components. The damage feeds on itself: fragmented collagen reduces the mechanical resistance of the extracellular matrix, lowering tension inside fibroblasts, which impairs their function and spurs further ROS production—a positive feedback loop that accelerates aging. ROS also oxidize DNA bases and break strands, and although repair pathways such as nucleotide excision repair and base excision repair normally respond, excessive oxidative stress can damage the repair machinery itself. Persistent DNA damage signalling activates ATM and ATR kinases, triggering the p53–p21 axis that locks cells into permanent cycle arrest and senescence, complete with the senescence-associated secretory phenotype.

The SASP is where individual senescent cells become a tissue-wide problem. Senescent cells resist apoptosis, evade immune clearance and broadcast inflammatory cytokines, growth factors and extracellular vesicles to their neighbours. Among the messengers, TGF-β normally drives collagen synthesis through Smad2/3 signalling, but photoaging reduces TGF-β receptor expression and UV radiation induces the inhibitory Smad7, choking off matrix production. IL-1α, stored in keratinocytes and released by UV exposure, activates the IRAK–TRAF6–TAK1 cascade, igniting NF-κB and inducing IL-6 and IL-8—while NF-κB in turn upregulates IL-1α, creating a self-amplifying inflammatory loop. Perhaps most striking are the extracellular vesicles: senescent cells release more of them, and these vesicles can carry toxic nuclear DNA fragments that induce senescence in recipient cells via the cGAS–STING pathway, as well as microRNAs such as miR-30a, miR-326-3p and miR-451a that suppress proliferation, promote fibroblast senescence and elevate ROS. Senescence, in effect, is contagious.

The review also highlights an epigenetic layer: histone modifications that govern macrophage polarization in aging wounds. The demethylase JMJD3 promotes early inflammatory M1 responses by removing the repressive H3K27me3 mark, but in diabetic wounds its sustained overexpression prolongs NF-κB-driven inflammation and delays healing. SETDB2-mediated H3K9me3 normally represses inflammatory genes and favours M2 polarization, yet it is downregulated in diabetic tissue. Persistent MOF-driven H4K16 acetylation sustains inflammatory transcription, and the age-associated histone lactylation mark H3K18La has been shown to activate NF-κB signalling at the promoters of p65 and p50. These findings suggest that aging skews the epigenetic landscape of immune cells in ways that trap wounds in a chronic inflammatory state, offering new targets for intervention.

On the therapeutic front, senotherapeutics lead the charge, divided into senolytics that kill senescent cells and senomorphics that neutralize their secretions. Navitoclax (ABT-263) inhibits anti-apoptotic BCL-2 family proteins, selectively eliminating senescent dermal fibroblasts, reducing MMP secretion and improving wound healing, though senescent melanocytes protected by MCL-1 resist it and side effects including thrombocytopenia demand caution. The flavonoids quercetin and fisetin induce apoptosis through PI3K/AKT inhibition, with the dasatinib–quercetin combination showing clinical promise for removing senescent fibroblasts, and fisetin additionally suppressing TNF-α, IL-1β, IL-6 and MMPs via NF-κB and MAPK/AP-1 blockade. Rutin, a senomorphic flavonoid, reduced wrinkle length and improved elasticity in a randomized double-blind trial while scavenging ROS and activating Nrf2 defences. Rapamycin suppresses the mTOR-driven SASP, enhances autophagy and directly activated TGF-β receptors in a trial showing increased dermal collagen and improved fine lines, while metformin activates AMPK to inhibit mTOR, reduce collagen-damaging oxidative stress and accelerate wound healing.

Stem cell therapy offers a complementary regenerative route. Mesenchymal stem cells can differentiate into keratinocyte lineages, and their secretomes—rich in GDF-11, TGF-β1, FGF family members, EGF, VEGF and HGF—stimulate fibroblast proliferation, collagen synthesis, angiogenesis and hair growth. Clinical trials using microneedling to deliver adipose-derived stem cell secretomes, umbilical cord-conditioned media and amniotic membrane preparations have reported significant improvements in wrinkles, elasticity, hydration and pigmentation. Stem cell-derived extracellular vesicles transfer TIMP1 to inhibit matrix-degrading enzymes, carry antioxidant peroxiredoxins and can push macrophages toward anti-inflammatory states. Delivery remains a bottleneck—the skin barrier limits penetration of most compounds—but liposomes, solid lipid nanoparticles, hydrogel-encapsulated systems and EV-based dual-loading carriers are extending how deeply and stably anti-aging agents reach their targets.

Perhaps the most forward-looking section concerns artificial intelligence. With traditional drug development slow and costly, machine learning models trained on labelled compound datasets are compressing discovery timelines dramatically. One XGBoost model screened more than 4,000 compounds and identified ginkgetin, periplocin and oleandrin as validated senolytics; an ensemble predictor combining a support vector machine and multilayer perceptron surfaced panaxatriol and voclosporin from hundreds of database candidates. The authors argue that integrating multi-omics data with AI could resolve the cellular heterogeneity that currently limits senolytic precision, though they caution that high-resolution spatial transcriptomic datasets for human skin remain scarce. For a field in which few candidates have reached Phase III trials, the convergence of senolytic chemistry, stem cell secretomes, nanoscale delivery and AI-driven screening may prove the combination that finally turns the biology of skin aging into treatable medicine.

Subject of Research: Molecular mechanisms of skin aging and emerging senotherapeutic, stem cell and AI-based interventions

Article Title: Skin Aging: From Molecular Mechanisms to Therapeutic and Technological Innovations

Article References: Chen, S., Yang, Y., Pan, X., Pan, Y., & Cai, S. (2026). Skin Aging: From Molecular Mechanisms to Therapeutic and Technological Innovations. Journal of Cellular and Molecular Medicine, 30(18), Article e71357. https://doi.org/10.1111/jcmm.71357

Image Credits: AI Generated

DOI: 10.1111/jcmm.71357

Keywords: skin aging, cellular senescence, SASP, senolytics, photoaging, reactive oxygen species, extracellular vesicles, macrophage polarization, mesenchymal stem cells, rapamycin, nanocarriers, machine learning

The biological rationale begins with reactive oxygen species, or ROS. These molecules, including superoxide anion, hydroxyl radical, and singlet oxygen, are unavoidable byproducts of oxidative metabolism, generated inside cells by electron leakage in mitochondria and outside them by ultraviolet radiation and pollution. At low levels, ROS act as legitimate signaling molecules in many cellular processes. But when their production outpaces the body’s antioxidant defenses, oxidative stress ensues, damaging DNA, proteins, and lipids, and driving cells toward apoptosis. The skin, as the body’s largest organ and its first line of contact with the environment, is particularly exposed. ROS accumulation triggered by ultraviolet light is considered a central event in photoaging, marked by collagen degradation, rupture of elastic fibers, and heightened activity of matrix metalloproteinases, the enzymes that dismantle the skin’s structural scaffolding.

Conventional skincare addresses oxidative stress with synthetic antioxidants and physical treatments, but these often irritate the skin, provoke photosensitivity, and deliver only temporary benefits. Natural antioxidants are generally less likely to cause irritation or allergy, and they align with the fast-growing consumer movement toward so-called clean beauty. What makes microalgae and cyanobacteria especially compelling is their evolutionary history. These are the oldest photosynthetic microorganisms on Earth, and populations living in hot springs, salt lakes, deserts, and high-irradiance intertidal zones have endured intense ultraviolet exposure, desiccation, and oxidative pressure for millions of years. Their response was to build elaborate chemical defenses, synthesizing structurally distinct antioxidants that terrestrial plants rarely produce, while also growing quickly and cultivable at scale on non-arable land.

The standout molecule is astaxanthin, a ketocarotenoid whose long chain of thirteen conjugated double bonds, capped by oxygenated ionone rings, gives it extraordinary capacity to quench singlet oxygen, outperforming other carotenoids as well as vitamins C and E. The green microalga Haematococcus pluvialis is the industrial workhorse, accumulating astaxanthin to five to eight percent of its dry cell weight, with annual production reaching tens of tons. In laboratory studies, concentrations of five to ten micromolar astaxanthin efficiently quenched UVA-induced ROS clusters in human dermal fibroblasts and lowered levels of malondialdehyde, a marker of lipid peroxidation. Mechanistically, astaxanthin also activates the cell’s own defenses: it promotes the release of the transcription factor Nrf2 from its cytoplasmic inhibitor Keap1, allowing Nrf2 to enter the nucleus and switch on genes for antioxidant enzymes such as glutathione S-transferases, glutathione peroxidase, superoxide dismutase, and NQO1.

Fucoxanthin, a polyunsaturated carotenoid with a reactive allenic bond and an epoxy group, delivers broad-spectrum radical scavenging and, in human keratinocytes, boosts glutathione through the same Nrf2 pathway. The diatom Phaeodactylum tricornutum and the haptophyte Tisochrysis lutea, which can reach nearly eighty milligrams of fucoxanthin per gram under optimized culture, are leading production candidates, and microalgae contain roughly ten to one hundred times more of the pigment than macroalgae. Beta-carotene, famously over-accumulated by the halotolerant green alga Dunaliella salina at up to fifteen percent of dry weight, quenches singlet oxygen through energy transfer and, in its 9-cis isomer form found uniquely in algae, exhibits strong antioxidant power. Lutein, currently harvested commercially only from marigold petals, could shift to algal sources that promise two to five times the per-hectare yield with eighty percent less water consumption and growth cycles as short as one to two weeks.

Beyond pigments, the review highlights polysaccharides, phycocyanin, polyphenols, mycosporine-like amino acids, and scytonemin as complementary actives. Sulfated exopolysaccharides from the red microalga Porphyridium cruentum and cyanobacterial EPS from Arthrospira and Nostoc scavenge radicals, chelate iron and copper ions that would otherwise fuel Fenton chemistry, and even form physical barriers against membrane lipid peroxidation. Phycocyanin, the brilliant blue pigment that makes up ten to twenty percent of Spirulina’s dry weight, directly eliminates ROS and reactive nitrogen species while enhancing intracellular antioxidant enzymes. Mycosporine-like amino acids, or MAAs, are especially elegant: these water-soluble molecules under four hundred daltons absorb UV-A and UV-B radiation with superb photostability, dissipating the energy harmlessly as heat rather than generating ROS, and compounds such as palythine and porphyra-334 rival ascorbic acid in radical-scavenging assays. Scytonemin, a lipophilic dimeric pigment produced in the extracellular sheaths of more than three hundred cyanobacterial species, absorbs across the UV-A, UV-B, and UV-C ranges.

What elevates these compounds above simple radical sponges is the breadth of their secondary effects on skin biology. Phycocyanin suppresses cyclooxygenase-2 and downstream prostaglandin E2, easing inflammation; fucoxanthin damps inflammatory cytokines through NF-kappaB signaling. On the anti-aging front, Spirulina polysaccharide complexes restore mitochondrial function in aged fibroblasts and spur collagen regeneration, while porphyra-334 increases procollagen, type I collagen, and elastin expression in UVA-irradiated skin fibroblasts. Several molecules inhibit the matrix metalloproteinases that degrade collagen and elastin: mycosporine-2-glycine from the halotolerant cyanobacterium Aphanothece halophytica matches the collagenase inhibitor aminoguanidine, C-phycocyanin reduces MMP-1 and MMP-9 in UVB-treated keratinocytes, and polysaccharides from Nostochopsis lobatus outperform the natural hyaluronidase inhibitor disodium cromoglycate. Microalgal polyphenols and phenolic acids also inhibit tyrosinase, the rate-limiting enzyme in melanin synthesis, offering safer alternatives to unstable or irritating whitening agents such as hydroquinone and kojic acid.

Commercial traction is already visible. Estee Lauder markets skincare lines featuring Chlorella extract for hydration and oil-water balance, while L’Oreal holds patents on marine polysaccharides for moisturizing and hair care. Astaxanthin appears in brightening serums and eye creams, and clinical trials suggest that oral doses of three to six milligrams per day reduce UV-induced wrinkles and enhance collagen synthesis. In the sunscreen space, Mibelle AG Biotechnology’s Helioguard 365, a porphyra-334 and shinorine complex from the red alga Porphyra umbilicalis, increased skin firmness by ten percent and reduced wrinkle depth by twelve percent over four weeks of application. Spirulina-derived extracts are found in anti-wrinkle and even antifungal formulations, and engineered microalgae-nanodrug delivery systems and live algal hydrogels are being explored for tissue repair, exploiting their capacity to produce oxygen through photosynthesis at wound sites.

Significant obstacles remain before these compounds reach their full potential. Extraction from tough algal cell walls is inefficient and often relies on polluting organic solvents, prompting interest in greener methods such as supercritical water extraction, ultrasound-assisted extraction, and enzyme-assisted processing. Stability is another vulnerability: carotenoids and phycobiliproteins degrade under light, heat, oxygen, and pH shifts, shortening shelf life, while hydrophilic and macromolecular ingredients struggle to cross the stratum corneum. Nanocarriers, including liposomes, nanoemulsions, and solid lipid nanoparticles, are emerging as solutions that shield actives and improve skin penetration, and the authors point to artificial intelligence-designed responsive delivery systems as a future frontier. Perhaps most critically, rigorous clinical evidence on biosafety, irritation, sensitization, and long-term effects remains thin for many novel species. The review calls for large-scale, multicenter, randomized, double-blind, placebo-controlled trials across diverse skin types and age groups, combined with omics-based mechanistic studies, to convert a promising laboratory story into the backbone of next-generation dermatological treatments and functional cosmeceuticals.

Subject of Research: Natural antioxidants from microalgae and cyanobacteria and their applications in skincare

Article Title: Natural antioxidants derived from microalgae and cyanobacteria and their applications in skincare

Article References: Natural antioxidants derived from microalgae and cyanobacteria and their applications in skincare. (n.d.). https://doi.org/10.1186/s44315-025-00050-w

Image Credits: AI Generated

DOI: 10.1186/s44315-025-00050-w

Keywords: microalgae, cyanobacteria, antioxidants, skincare, astaxanthin, phycocyanin, mycosporine-like amino acids, carotenoids, photoaging, Nrf2 pathway, sunscreen, cosmetics

The research team focused on two of the most common plastics in consumer products and packaging: polypropylene, known as PP, and polymethyl methacrylate, known as PMMA. Both were obtained in four colors: red, yellow, blue, and green. Before any testing, the particles were characterized in their virgin state, and then the team subjected them to controlled aging designed to mimic the ultraviolet radiation and oxidative stress that plastics experience in sunlit surface waters. Aging is not a cosmetic process. As polymer chains break under photochemical attack, surfaces crack, oxygen-containing functional groups accumulate, and particle dimensions shrink, all of which change how a fragment interacts with dissolved molecules in its surroundings.

The physical consequences of aging turned out to be strikingly color-dependent. Under microscopic examination, aged red polypropylene developed a dense network of wrinkles across its surface, while blue polypropylene responded differently, showing irregular flaking in which small pieces of the weathered surface peeled away. These distinct degradation morphologies imply that pigments do not merely sit inertly inside the polymer matrix; they alter how the material absorbs light, generates reactive species, and ultimately disintegrates. Particle size measurements confirmed that aging matters quantitatively as well as visually. Across the polypropylene samples, the average particle size decreased by 6 to 30 percent after aging, with red and yellow particles showing even greater reductions than the overall average, indicating that those pigments either accelerate photodegradation or produce more fragile weathered surfaces.

With the aged and virgin particles in hand, the researchers turned to the central question of the study: how do these differently colored, differently weathered plastics adsorb tetracycline hydrochloride, the hydrochloride salt form of the antibiotic commonly used in medicine and in intensive livestock farming. Tetracycline is a useful probe pollutant because it carries multiple ionizable groups, meaning its charge state shifts with the acidity of the surrounding water, and it can engage plastics through hydrogen bonding, electrostatic attraction, and other surface interactions. Adsorption onto microplastics matters environmentally because particles that soak up antibiotics can transport them far from their point of release, potentially concentrating the drugs in the tissues of organisms that ingest the particles and fostering antibiotic resistance along the way.

The adsorption results revealed a clear hierarchy among the colors that shifted after weathering. For virgin microplastics, the adsorption capacity followed the order red greater than blue greater than yellow approximately equal to green. After aging, the ranking rearranged itself to red greater than yellow approximately equal to green greater than blue, with the yellow and green particles showing significant improvements in adsorption performance. In other words, weathering did not simply boost every color equally; it reshuffled the leaderboard. Red polypropylene remained the strongest binder both before and after aging, but blue particles, which had held second place in their pristine state, dropped to the bottom of the pack once weathered. This reordering demonstrates that the pigment-driven degradation pathways interact with the surface chemistry changes that aging induces, producing net outcomes that cannot be predicted from either factor alone.

The study also examined how two master variables of aquatic chemistry, pH and ionic strength, modulate these interactions. For virgin polypropylene, adsorption of tetracycline hydrochloride reached its maximum at pH 9, whereas aged polypropylene achieved its maximum at pH 7, near neutral conditions. That shift matters because natural freshwaters span a range of pH values, and a weathered particle that binds antibiotics most strongly at neutral pH will behave very differently in a river than a fresh fragment that prefers alkaline conditions. For PMMA, the picture was simpler: maximum adsorption capacity occurred at pH 5 both before and after aging, suggesting that this acrylic polymer’s surface chemistry responds to acidity in a way that is more robust to weathering than polypropylene’s.

Ionic strength produced its own characteristic pattern. Low concentrations of sodium chloride enhanced the adsorption capacity of the colored microplastics, but as the salt concentration increased further, adsorption declined. This non-monotonic response likely reflects competing effects of dissolved ions on the electrical double layers surrounding both the plastic surfaces and the tetracycline molecules, as well as on the antibiotic’s own speciation. Because salinity varies enormously across environments, from soft freshwater streams to brackish estuaries and open seawater, the result implies that the same fragment of colored plastic could act as a strong or weak antibiotic carrier depending on where it drifts. For risk modelers, the message is that color, weathering history, pH, and salinity must be considered jointly rather than as isolated factors.

Why would color exert such power over a polymer’s environmental chemistry? The authors point to the role of pigments in mediating photodegradation. Different pigments absorb different portions of the light spectrum, and some can act as photosensitizers that accelerate the formation of reactive oxygen species within the polymer, while others may shield the matrix or promote specific failure modes such as the flaking seen in blue polypropylene. Prior work by the same group, published in the Journal of Contaminant Hydrology, showed that microplastic color influences the release of dissolved organic matter during photoaging, and earlier studies on polyvinyl chloride found that color affects biofilm development and the chemodynamics of heavy metals on plastic surfaces. The new results extend that theme to antibiotic adsorption on two additional polymers, strengthening the case that color is a first-order variable in microplastic science rather than a cosmetic footnote.

The broader implications reach into public health and environmental policy. Antibiotic pollution drives the evolution of resistance genes, and microplastics are increasingly recognized as vectors that can carry both antibiotics and resistant bacteria through water systems, as documented in studies of plastisphere communities and biofilm-antibiotic interactions. If red and yellow weathered polypropylene bind tetracycline more strongly than other colors, then fragments from red agricultural film, packaging, or consumer goods may pose disproportionate risks in watersheds affected by pharmaceutical runoff. The authors state that their findings provide a theoretical basis for assessing the ecological risks posed by different colored microplastics in complex pollution scenarios, and the work was supported by the Natural Science Foundation of Anhui Province, the Engineering Research Center of Biofilm Water Purification and Utilization Technology of the Ministry of Education, and Anhui University of Technology’s Innovation Training Program.

For now, the study stands as a reminder that the plastic pollution crisis is more chemically intricate than it appears. Two particles of identical polymer type, size, and shape can behave entirely differently in a river if one is red and the other is blue, and both will change again after months of sunlight. As monitoring programs worldwide begin quantifying microplastics in drinking water sources, groundwater, and agricultural soils, incorporating color as a measurable parameter alongside polymer identity and weathering state could sharpen the accuracy of exposure models. The next step, the researchers suggest, is applying this theoretical basis to real-world mixtures, where colored microplastics, antibiotics, salts, and shifting pH coexist, and where the humble pigment inside a fragment of plastic may quietly decide how much of humanity’s pharmaceutical burden hitchhikes through the environment on its surface.

Subject of Research: Color-dependent aging and adsorption of tetracycline by polypropylene and PMMA microplastics

Article Title: Color-Dependent Adsorption Behavior of Tetracycline onto Aged Microplastics

Article References: Jin, R., Li, X., Li, M., & Shen, M. (2026). Color-Dependent Adsorption Behavior of Tetracycline onto Aged Microplastics. Archives of Environmental Contamination and Toxicology, 91(3), Article 19. https://doi.org/10.1007/s00244-026-01221-5

Image Credits: AI Generated

DOI: 10.1007/s00244-026-01221-5

Keywords: microplastics, polypropylene, PMMA, tetracycline, adsorption, photoaging, plastic color, pH, ionic strength, antibiotic pollution, ecological risk, Color-Dependent