The rapid rise of glucagon-like peptide-1 receptor agonists, or GLP-1 RAs, is transforming the treatment of obesity—and exposing a problem that medicine has struggled to solve for decades. These drugs can reduce appetite, alter food-reward pathways and improve several cardiometabolic measures, including blood-glucose control and cardiovascular risk factors. Their popularity has surged across clinical practice, private health services and, increasingly, self-directed online markets. But a new commentary in BMC Medicine argues that the medication revolution will not deliver its full promise unless it is paired with sustained psychological, behavioral and social support. Brunna Boaventura of the Federal University of Santa Catarina in Brazil and Stuart W. Flint of the University of Leeds in the UK warn that prescribing medication without helping people build durable behavior-change skills could create a modern version of an old mistake: treating body weight as an isolated problem rather than as one part of a complex chronic disease.

The authors’ central message is not that lifestyle interventions should replace medication. Instead, they argue that obesity care must become genuinely multimodal, combining pharmacological treatment with structured behavioral support and, when appropriate, psychological, nutritional, medical and surgical care. The World Health Organization recognizes obesity as a chronic, relapsing disease, meaning that long-term management is often necessary even after substantial weight loss. Yet in routine healthcare, behavioral treatment is frequently reduced to brief advice—“eat better,” “exercise more” or “monitor your weight”—rather than delivered as a continuous clinical service. That implementation gap has several causes: many clinicians receive limited training in behavior-change techniques, referral routes to dietitians, psychologists and health coaches may be weak, reimbursement is often inadequate, and healthcare systems rarely account for the social and structural conditions that shape daily choices. The result is a mismatch between the biological complexity of obesity and the simplicity of the support many patients receive.

GLP-1 RAs make that mismatch more consequential because their benefits are closely tied to continued treatment and individual response. The drugs mimic or enhance signaling by hormones involved in appetite regulation and glucose metabolism. By activating GLP-1 receptors, they can slow gastric emptying, increase feelings of fullness and reduce food intake; their metabolic effects can also improve glycemic control. But these physiological changes do not automatically resolve the habits, routines, emotional triggers, social pressures or practical barriers that influence eating and physical activity. Nor do they guarantee identical outcomes for every patient. Some people respond strongly, others less so, and side effects, cost or limited availability can lead to treatment interruption. A systematic review and meta-analysis cited by Boaventura and Flint examined 37 studies involving 9,341 participants and found that weight regain after stopping obesity medication occurred faster than regain following behavioral weight-management programs, regardless of the amount of weight initially lost. The finding does not mean medication is ineffective; it shows why medication should be embedded in a plan designed for continuity and adaptation.

Behavior change is not a matter of receiving information and then demonstrating sufficient willpower. It emerges from the interaction of cognitive processes, emotions, motivation, self-regulation and the environment in which a person lives. An individual may intend to change eating patterns but face irregular work schedules, food insecurity, chronic stress, limited access to safe exercise spaces or a history of negative experiences in healthcare. Motivation itself can fluctuate, while habits are often triggered by cues that operate outside conscious awareness. Effective support therefore involves more than education. It can include collaborative goal setting, monitoring progress, identifying barriers, developing coping strategies, reinforcing self-efficacy and adjusting plans as circumstances change. Such interventions are most effective when they are person-centered: goals should reflect health, functioning and quality of life, not only the number on a scale. The authors say this broader approach is essential as drug-centered models become more common, because a prescription can influence appetite without supplying the skills and support needed to sustain health-related behaviors over years.

The commentary places weight stigma at the center of this challenge. People living with obesity frequently encounter moral judgment in clinics, workplaces, media and everyday life, where body size is often interpreted as evidence of laziness, irresponsibility or poor character. Those experiences can produce internalized weight stigma—the adoption of negative cultural beliefs about one’s own body—which is associated with distress, reduced self-confidence and disengagement from care. A clinical encounter that focuses narrowly on weight loss may unintentionally intensify the problem, particularly when treatment success is defined by a predetermined percentage of weight reduction. By contrast, addressing stigma and its consequences can improve eating self-efficacy, quality of life, treatment acceptability and patients’ ability to cope with difficult experiences. The authors argue that behavior-change support should therefore help people manage not only diet and physical activity, but also shame, discrimination, body-image concerns, fears of regain and the psychological burden of being judged.

The arrival of GLP-1 medications has produced a complicated cultural shift. On one hand, the drugs may challenge the idea that obesity is simply a failure of self-control by highlighting the roles of appetite, satiety, food reward and biological regulation. On the other hand, people who use them may still be criticized for taking what some regard as a shortcut. Research cited in the commentary suggests that GLP-1 use can influence how women with different body weights are evaluated, but the authors caution against assuming that medication automatically removes stigma. A person may lose weight and still carry years of negative self-beliefs, altered body image or anxiety about returning to a previous size. Physical change can itself require psychological adjustment, especially when identity, relationships and social treatment have been shaped by body weight. These consequences may persist even when a medication is working medically. In that sense, successful obesity care must address the lived experience of treatment rather than treating weight reduction as the sole endpoint.

Existing behavioral programs may not be broad enough for this new era. The intensive behavioral therapy model covered by the US Centers for Medicare & Medicaid Services emphasizes diet, physical activity and self-monitoring, with delivery largely centered on physicians and nurses and success commonly tied to weight-loss thresholds. Those components can be useful, but Boaventura and Flint argue that a weight-centered framework overlooks outcomes that matter to patients and health systems, including cardiometabolic health, mobility, mental well-being, quality of life and quality-adjusted life years. It may also fail to include professionals with specialized expertise in counseling, psychology, nutrition and sustained coaching. A broader model would measure whether people can maintain beneficial routines, manage distress, participate more fully in daily life and reduce health risks—even when weight loss is modest or fluctuates. This distinction is scientifically important because body weight is only one observable outcome of a treatment, while metabolic health and psychological functioning may change along different trajectories.

The risks become sharper when access to regulated care is limited. Demand, cost and shortages have encouraged some people to seek GLP-1 RAs through online sellers, private services or self-directed pathways. Such routes can separate medication access from clinical assessment, dose monitoring, side-effect management and follow-up. They may also expose patients to counterfeit or falsified products, inappropriate prescribing and fragmented care. When obtaining the drug becomes the primary objective, behavioral and psychosocial support can be treated as optional extras rather than essential parts of treatment. The authors do not suggest that every patient must receive an identical package of services, but they insist that safe care requires more than dispensing a medication. Patients need reliable information, supervision and access to appropriately trained professionals who can help them respond to changing appetite, adverse effects, treatment interruptions and the possibility of weight regain. Regulation, they argue, should focus not only on the products themselves but also on whether the surrounding service provides comprehensive care.

The policy implications extend beyond individual consultations. Multidisciplinary obesity treatment is widely recommended, yet it remains difficult to obtain in both public and private systems. Public-health programs need investment so that integrated services are available beyond specialist centers, while private care must confront the financial barriers created when several professionals and an expensive medication are combined. Health systems and regulators should ensure that obesity services include behavioral, psychological and social support, rather than allowing pharmacotherapy to become a substitute for chronic-care infrastructure. The authors describe this as an opportunity to redesign obesity treatment around empowerment and long-term health. GLP-1 RAs may be powerful tools, but they cannot by themselves teach people how to navigate stigma, stress, disrupted routines or the emotional consequences of bodily change. The future of obesity medicine, the commentary concludes, will be determined not simply by how many people receive these drugs, but by whether healthcare can surround them with the sustained, person-centered support required to make improvement safer and more durable.

Polypharmacy is often associated with older adults and people living with several chronic diseases, but it can occur whenever multiple conditions, symptoms or treatment guidelines converge. A patient may receive separate medicines for hypertension, diabetes, pain, infection or gastrointestinal symptoms, while different clinicians may prescribe without a complete view of the person’s current regimen. Some combinations are medically necessary and can improve survival or disease control. The concern arises when medicines are duplicated, continued after their original indication has disappeared, prescribed without adequate monitoring, or used in combinations whose benefits do not outweigh their risks. The biological challenge is cumulative: each medicine can produce intended effects as well as side effects, and one drug may alter the absorption, metabolism or elimination of another. As the number of medicines rises, the possible interaction pathways multiply, making careful medication reconciliation and periodic review increasingly important.

The Nigerian research used two complementary approaches. First, the investigators retrospectively examined 2,000 prescriptions issued between January and June 2025 to estimate how frequently patients were receiving multiple medicines. They then conducted a prospective questionnaire survey from July through August involving 100 patients and 50 healthcare providers. The prescription review provided a numerical snapshot of prescribing patterns, while the questionnaires explored the financial consequences for patients and the perceptions of professionals working in the hospital. This design allowed the team to connect prescribing complexity with reported affordability problems, although it cannot establish that polypharmacy itself caused patients to reduce their medicines. The study was cross-sectional in its survey component, meaning that it captured experiences over a defined period rather than tracking patients over time to determine whether medication changes led to later complications or hospital visits.

Of the prescriptions examined, 63 percent contained two to four medicines, a range the researchers classified as non-polypharmacy for the purposes of the study. Another 25 percent contained five to nine medicines, described as major polypharmacy, while 12 percent contained at least 10 medicines, categorized as excessive polypharmacy. Taken together, the latter two groups accounted for 37 percent of all prescriptions. These figures do not necessarily mean that 37 percent of patients were receiving inappropriate treatment. A prescription containing several medicines may be clinically justified, particularly for patients with multiple chronic conditions or acute illness. The study instead identifies the scale of medication exposure and the need to determine whether each medicine remains necessary, effective and affordable. Without detailed diagnoses, treatment indications and clinical outcomes for every prescription, the data cannot distinguish appropriate combination therapy from potentially avoidable prescribing.

The financial findings were especially striking. Among the 100 patients who completed questionnaires, 37 percent reported spending more than 20,000 Nigerian naira per month on medicines. The researchers did not convert that amount into a universal international comparison, because the real impact depends on household income, local prices and other living costs, but the responses show that medication expenditure was not a marginal concern. Seventy-nine percent of participants described drug costs as a financial burden, and 78 percent said they needed financial assistance to obtain the medicines prescribed for them. In a predominantly out-of-pocket healthcare environment, the price of each additional product can become a barrier to completing treatment. Patients may borrow money, rely on relatives, purchase only part of a prescription or substitute medicines without professional guidance, creating a cycle in which the intended therapeutic plan is never fully implemented.

The researchers found that 66 percent of surveyed patients had skipped doses or reduced their medicines because of cost. This behavior, known as cost-related nonadherence, can undermine treatment even when the prescription is pharmacologically sound. For medicines used to control blood pressure or blood glucose, intermittent dosing may produce unstable disease control rather than a simple reduction in benefit. For antimicrobial treatment, taking medicines inconsistently can fail to clear an infection, although the relationship between adherence and antimicrobial resistance is complex and depends on the drug, pathogen and treatment regimen. Reducing or skipping medicines can also make clinicians interpret uncontrolled symptoms as evidence that a treatment is ineffective, potentially prompting additional prescriptions and increasing polypharmacy further. The result is a dangerous feedback loop: more medicines raise costs, high costs reduce adherence, and poor adherence may lead to even more intensive treatment.

Healthcare providers surveyed in the study recognized the same pattern from the clinical side. Eighty-four percent said they frequently encountered patients taking five or more medicines, and every provider agreed that polypharmacy significantly increases treatment costs. Clinicians may face genuine pressure to address several problems during a single consultation, particularly in facilities serving communities with limited access to specialist care. Prescribing can also be shaped by fragmented records, limited consultation time, patient expectations and the availability of medicines. A complete medication review requires more than asking whether a patient is taking tablets. It involves identifying every prescription, over-the-counter product, traditional remedy and supplement; checking dose, duration, indication and duplication; considering kidney and liver function; and evaluating whether the patient can follow the schedule. Pharmacists, physicians and nurses can work together to simplify regimens, select lower-cost equivalents when appropriate and stop medicines whose risks exceed their benefits.

The study’s implications extend beyond one hospital. Nigeria, like many low- and middle-income countries, must manage rising burdens of chronic disease while healthcare financing remains uneven. As people live longer and survive illnesses that once would have been fatal, the number of patients requiring long-term treatment is likely to grow. At the same time, medicine prices, transport costs and shortages can place therapy beyond reach. Expanding health insurance coverage could reduce the direct financial shock of multiple prescriptions, but insurance alone would not solve inappropriate or unnecessarily complex treatment. The authors point to rational prescribing and strengthened medication-review practices as parallel solutions. Rational prescribing means selecting a medicine that matches a clearly defined clinical need, at the correct dose and duration, while considering safety, effectiveness, affordability and the patient’s ability to use it. Electronic prescribing systems and shared records could help, but even paper-based review protocols may identify duplication and unnecessary continuation.

The findings should nevertheless be interpreted with care. The study was conducted in a single secondary healthcare facility, so its prescribing patterns may not represent hospitals elsewhere in Nigeria or other healthcare levels. The patient survey included only 100 participants, and information about spending, skipped doses and financial assistance was self-reported, which can introduce recall or reporting bias. The researchers also measured the number of medicines rather than documenting adverse drug reactions, hospital admissions, disease outcomes or the clinical appropriateness of each combination. Further research across multiple facilities could examine which diseases and prescribing departments contribute most to polypharmacy, how much of the medication burden is clinically justified, and whether pharmacist-led reviews reduce costs without harming health outcomes. Even with these limitations, the central signal is clear: when 37 percent of prescriptions contain five or more medicines and most surveyed patients struggle to pay for them, medication management becomes both a safety issue and an economic one. The challenge is not merely to prescribe fewer drugs, but to ensure that every medicine a patient receives has a defensible purpose, a measurable benefit and a realistic path to completion.

B cells hold a privileged role within the immune system, not solely as antibody factories but as multifaceted regulators of immune responses. Their capacity to engage in intricate cellular dialogues extends beyond humoral immunity, involving modulation of T cells and influencing other immune compartments. This ability, coupled with a naturally long lifespan and prolific protein production machinery, positions B cells as a powerful platform for delivering therapeutic proteins in a sustained and controlled fashion. By genetically reprogramming these cells, scientists hope to transform B cells into living drug factories that can precisely target pathological processes within the body.

The breakthrough came with the advent of highly efficient genome editing tools such as CRISPR-Cas systems, which facilitate targeted insertion, deletion, or modification of specific genes within B cells. These advances have overcome previous obstacles related to gene delivery and manipulation in primary B cells, which traditionally displayed resistance to genetic engineering. Leveraging electroporation techniques and viral vectors optimized for B cell transduction, researchers have now established robust workflows to engineer B cells ex vivo before reintroducing them to the patient’s body, thereby conferring a new therapeutic identity.

Animal models have played an indispensable role in validating the feasibility and efficacy of eB cell therapies. Genetically humanized mice, along with advanced immunodeficient strains, allow detailed dissection of eB cell functions within complex immunological environments mirroring human physiology. These models have provided invaluable insights into the persistence, homing, and immunomodulatory effects of engineered B cells, setting the foundation for rational design of clinical interventions. Importantly, they enable monitoring of potential adverse effects such as off-target activity or immune rejection, which are critical considerations for ensuring safety in translational applications.

The clinical translation of eB cell therapy has already entered a nascent stage, with early-phase trials testing the capacity of engineered B cells to produce therapeutic antibodies targeting infectious diseases and autoimmune disorders. Preliminary results demonstrate promising safety profiles and durable protein expression, suggesting that eB cells can overcome many limitations faced by traditional biologics, such as repeated dosing and immunogenicity. These pioneering studies not only validate the concept but also provide a roadmap for expanding the therapeutic arsenal based on engineered lymphocytes.

One of the most captivating aspects of eB cell therapies lies in their versatility. Unlike static drugs or monoclonal antibodies, engineered B cells can potentially adapt to changing disease landscapes by responding to endogenous cues or external control signals introduced by synthetic biology circuits. This dynamic responsiveness could allow precision timing and dosing of therapeutic protein release, minimizing systemic side effects while maximizing efficacy. Moreover, integrating suicide switches or safety switches mitigates risks linked to uncontrollable cellular proliferation or off-target immune activation, enhancing the clinical attractiveness of these living therapeutics.

Despite the mounting enthusiasm, substantial hurdles remain before eB cell therapies become mainstream treatments. Manufacturing complexities, including the isolation, expansion, and genetic modification of high-quality autologous B cells, require scalable and reproducible protocols that meet stringent regulatory standards. Furthermore, understanding the long-term behavior of engineered B cells within diverse patient populations is crucial to anticipate issues related to clonal expansion, immunological tolerance, and potential oncogenic transformations. These scientific and manufacturing challenges necessitate collaborative efforts bridging immunology, bioengineering, and clinical disciplines.

Future applications envision leveraging engineered B cells not only as protein delivery vehicles but also as diagnostic and research tools in immunology and oncology. For example, eB cells could be programmed to sense specific antigens or inflammatory signals, thereby functioning as living biosensors capable of reporting or modulating immune responses in real time. This dual role—as both therapeutics and investigational instruments—could revolutionize personalized medicine by enabling adaptive interventions tailored to individual disease trajectories.

The convergence of synthetic biology with immunotherapy is gradually dismantling traditional boundaries, illustrating how fundamental insights into B cell biology can be translated into transformative treatments. Advances in single-cell sequencing and proteomics have elucidated the heterogeneity and plasticity of B cell populations, informing rational engineering strategies to enhance their therapeutic potential. By exploiting these underlying mechanisms, therapeutic programs can be fine-tuned to optimize protein secretion profiles, cellular lifespan, and immunomodulatory functions, ultimately leading to safer and more effective treatments.

Recent data also highlight the importance of microenvironmental factors in dictating eB cell functionality and persistence. Tissue niches such as the spleen, bone marrow, and lymph nodes provide signals that influence survival and differentiation states of B cells, thereby affecting therapeutic outcomes. Understanding these interactions empowers the design of eB cells engineered to exploit or resist local cues, ensuring sustained activity and targeted localization. Additionally, innovations in biomaterials and delivery platforms could synergize with eB cells to create composite therapies that orchestrate complex immune responses against tumors or chronic infections.

The potential of eB cells extends into oncology, where B cells can be armed to secrete tumor-specific antibodies or immune-modulating cytokines within tumor microenvironments, overcoming barriers encountered by conventional antibody therapies and checkpoint inhibitors. By combining antigen specificity with controlled protein production, these engineered cells promise to mount robust and durable antitumor responses, potentially surmounting immune evasion mechanisms employed by cancers. Early preclinical efforts demonstrate encouraging efficacy in hematological malignancies, laying the groundwork for future solid tumor applications.

Similarly, chronic inflammatory conditions such as autoimmune diseases could benefit from eB cell strategies that deliver anti-inflammatory cytokines or immune tolerance-inducing molecules directly at sites of active inflammation. This localized immunosuppression could minimize systemic immunosuppression risks, preserving host defense mechanisms. The flexibility to design antigen-specific regulatory B cells opens avenues for disease-modifying therapies that not only alleviate symptoms but also address root causes of autoimmunity by restoring immunological balance.

Beyond therapeutic contexts, engineered B cells are becoming instrumental in advancing our understanding of immune system dynamics. By manipulating signaling pathways and effector functions within B cells, researchers can model disease states and unravel pathological mechanisms with unprecedented precision. This experimental leverage facilitates high-throughput screening of novel immunomodulatory agents and accelerates the discovery pipeline, reinforcing the bidirectional relationship between engineered cellular therapies and fundamental immunological research.

In summary, the engineering of B cells ushers in a new chapter in cell therapy development, characterized by the exploitation of natural biological properties to create highly customizable and potent therapeutic platforms. The translational journey from bench to bedside is underway, supported by technological breakthroughs that enable precise genetic manipulation and sophisticated models that predict clinical behavior. As the field matures, interdisciplinary collaborations will be essential to fully realize the promise of eB cell therapies, transforming them from visionary concepts into practical tools combating cancer, chronic diseases, and beyond.

Subject of Research: Engineering B cells for therapeutic applications and disease modeling through genome editing and immunological techniques.

Article Title: Engineering B cells to treat and study human disease.

Article References:
Trivedi, N., Pitner, R.A., Rawlings, D.J. et al. Engineering B cells to treat and study human disease. Nat Biotechnol (2025). https://doi.org/10.1038/s41587-025-02757-y

Image Credits: AI Generated

Traditionally regarded as a lymphoid organ primarily involved in blood filtration and immune surveillance, the spleen has long been underestimated for its regenerative potential. The research team, led by Professors Lei Dong and Jian Xiao, challenged this dogma by engineering a microenvironment within the spleen that supports not only cell survival but also functional maturation of transplanted human islets. This approach circumvents two critical obstacles that have historically limited the success of islet transplantation: poor cell survival due to inadequate extracellular support and immune-mediated graft rejection.

At the core of their innovation lies the deployment of sophisticated immunomodulatory nanoparticles designed to reprogram the spleen’s microenvironment. These nanoparticles enhance the extracellular matrix, promote angiogenesis, and create an immunosuppressive milieu, which collectively orchestrate a niche conducive to islet engraftment and functionality. By modifying the spleen’s local immune responses and tissue architecture, the researchers converted this once overlooked organ into a bioengineered hub where transplanted cells can not only survive but integrate and proliferate.

This reprogramming effort facilitated the survival and functional maturation of human islet tissues inside the spleens of cynomolgus macaques, non-human primates that serve as an essential preclinical model. Remarkably, the spleen exhibited compatibility with both xenogeneic (human) and allogeneic (animal) cell sources, underscoring the platform’s versatility and its potential to address organ shortages through cross-species transplantation strategies. This breakthrough signals a new paradigm, wherein the spleen is utilized as a living factory to cultivate organ-specific cells within the host, minimizing the complications associated with external organ transplantation.

The biological rationale for selecting the spleen is rooted in its intrinsic characteristics. Its porous and spacious architecture can accommodate billions of cells, providing a structurally supportive scaffold. Moreover, the spleen’s direct blood flow into the liver’s portal vein system offers a nutrient-rich, physiologically relevant environment akin to natural developmental settings for islet cells. Finally, the organ’s capacity to undergo remodeling without compromising systemic homeostasis makes it an ideal candidate for repeated therapeutic interventions.

The research is not an isolated achievement but the continuation of a series of pioneering studies by the team. Earlier work demonstrated that mouse spleens could be reprogrammed to assume liver functions, exemplified in their 2020 Science Advances publication. Subsequently, in 2022, they successfully grew liver tissues in situ using gene-editing technologies, bypassing the need for exogenous cell transplantation. More recently, they rebuilt hormone-secreting thyroid tissues within animal spleens, showcasing the platform’s adaptability for diverse organ systems. This cumulative evidence solidifies the spleen’s role as a multi-organ regeneration factory within the mammalian body.

Looking forward, the investigators are exploring the integration of induced pluripotent stem cells (iPSCs) into their spleen bioreactor model to realize patient-specific organogenesis. This strategy envisages harvesting a patient’s own reprogrammed stem cells, delivering them via minimally invasive ultrasound-guided techniques into the spleen, and nurturing fully functional organs tailored to the individual’s immunological profile. Such personalized regenerative therapy could obviate lifelong immunosuppression and dramatically elevate transplant success rates.

Clinically, the transition from experimental models to human applications will necessitate a stringent evaluation of biosafety, efficacy, and long-term functional outcomes. Immune tolerance, potential off-target effects of nanoparticle delivery, and sustained organ performance remain pivotal challenges to address. Nevertheless, this research fundamentally challenges prior assumptions about the spleen’s dispensability and harnesses its latent potential to redefine the future landscape of organ replacement therapies.

Professors Dong and Xiao’s vision encapsulates a transformative concept of the spleen—not just as an immune organ but as a versatile bioreactor embedded within the human body, silently manufacturing life-saving tissues on demand. Their method converges advanced nanotechnology, tissue engineering, and immunology in a highly sophisticated platform that could eventually eliminate the organ shortage crisis and revolutionize treatment options for diabetics and patients with organ failure worldwide.

This emerging paradigm aligns with the broader goals of regenerative medicine: to create endogenous platforms where damaged or deficient tissues are repaired or replaced within the patient’s own body, thereby reducing complications from immunorejection and improving quality of life. This study exemplifies the power of interdisciplinary collaboration and innovation, shining a new light on an organ once believed secondary but now revealed as a cornerstone for future regenerative therapies.

The scientific community and healthcare providers alike will watch closely as this research continues to evolve, with anticipation that it will catalyze a wave of organ bioengineering advances. The spleen, a long-overlooked player in systemic physiology, now stands at the cusp of transforming not only how we understand organogenesis but also how medicine approaches tissue failure, heralding a future where bespoke, in-body organ factories become a clinical reality.

Subject of Research: Animals

Article Title: Islet transplantation in immunomodulatory nanoparticle–remodeled spleens

News Publication Date: 21-May-2025

Web References: http://dx.doi.org/10.1126/scitranslmed.adj9615

Image Credits: Credited by Lei Dong/Nanjing University and Jian Xiao/Wenzhou Medical University

Keywords: Cell biology