“This collection is published in memory of Professor Judith Campisi, a pioneering force in the field of cellular senescence whose groundbreaking work shaped the understanding of senescence in aging, cancer, and tissue homeostasis.”
BUFFALO, NY — May 1, 2025 —Aging (Aging-US) invites submissions for a Special Collection dedicated to the theme of cellular senescence, spanning its basic mechanisms, physiological and pathological functions, and clinical applications.
This collection is published in memory of Professor Judith Campisi, a pioneering force in the field of cellular senescence whose groundbreaking work shaped the understanding of senescence in aging, cancer, and tissue homeostasis. Her legacy continues to inspire generations of scientists working to decode the complex biology of senescent cells and their impact on health and disease.
We welcome original research articles, reviews, and perspectives on topics including:
Fundamental mechanisms of senescence induction and maintenance
Regulation and context-specific roles of the senescence-associated secretory phenotype (SASP)
Beneficial and detrimental effects of senescent cells in vivo
Senescence in development, aging, regeneration, and age-related diseases
Biomarkers, imaging, and tools for senescence detection and quantification
Therapeutic targeting of senescent cells: senolytics, senomorphics, and clinical translation
This Special Collection is guest edited by Han Li and Irina Conboy, both internationally recognized leaders in the study of senescence and aging.
This important event brought together 350 participants—chosen from more than 1,300 applicants—including students, researchers, company founders, investors, and industry leaders. Together, they explored the latest research and innovations in muscle health and aging. The symposium reflected the journal’s strong commitment to supporting collaboration across fields and advancing research in aging.
The panel discussed key topics such as the biology of frailty, how bone and muscle health are connected, and the influence of genetics, diet, and exercise on staying strong as we age. By blending real-life patient care with the latest research, the speakers shed light on the challenges of sarcopenia—the gradual loss of muscle strength and mass that occurs with age—and the new scientific approaches being developed to improve treatment.
Next-Generation Therapeutic Approaches
Lada Nuzhna, founder and CEO of Stealth Newco and director at Impetus Grants, shared her vision for advancing muscle health through innovation. With a strong focus on translational impact, she discussed her interest in developing a comprehensive program that combines various exerkines—exercise-induced signaling molecules—to improve muscle function.
Dr. Francisco Leport, co-founder and CEO of Gordian Biotechnology, introduced a new method for studying treatments for osteoarthritis, a common age-related joint condition that causes pain and stiffness. His approach, called in vivo pooled screening, allows scientists to test millions of potential therapies inside a single animal with the disease. This technique speeds up research and reduces the need for using multiple animals, helping to move from discovery to treatment more quickly.
Biotech and Drug Development for Muscle Aging
This panel brought together leading voices from Lilly (Dr. Andrew Adams), Novartis (Dr. Anne-Ulrike Trendelenburg), Regeneron (David Glass, MD), and Versanis Bio (Ken Attie, MD). Together, they explored therapeutic strategies focused not just on lifespan extension but on preserving mobility, muscle function, and independence as people age.
The discussion emphasized a human-centric approach to drug development, focusing on targeting mechanisms quickly and efficiently in clinical studies, and the importance of early intervention to achieve larger effect sizes and better long-term outcomes. Panelists also stressed that muscle function matters more than mass and highlighted how older individuals often experience a loss of mitochondrial function, leading to fatigue and reduced stamina—underscoring the need for programs that support mitochondrial health.
The panel further noted that nerve decline may precede muscle decline with age. While there is no definitive data linking cognitive and muscle function, improvements in vascular health through exercise were highlighted as a way to reduce inflammation and support overall health. In addition, they addressed the rise of GLP-1-based therapies, including the public health concern of weight regain following treatment.
Exercise Science for Muscle Longevity
This energizing final session featured Dr. Brad Schoenfeld from Lehman College and Dr. Jeff Nippard, a professional bodybuilder, powerlifter, and science communicator. Together they shared research-backed strategies for preserving muscle health at any age, emphasizing that it is never too late to start training and that even minimal, consistent exercise can significantly boost mobility and independence. They also recommended incorporating power and explosive movements into workouts and emphasized the importance of adequate leucine intake to support muscle health.
Driving Scientific Progress in Muscle and Aging Research
The MAST Symposium, like previous Aging Initiative at Harvard University events, showcased the power of interdisciplinary collaboration, mentorship, and early engagement in driving scientific progress. Aging (Aging-US) is proud to support initiatives that highlight the latest breakthroughs while inspiring younger generations to pursue meaningful careers in aging research.
From innovative drug development to accessible exercise interventions, the MAST Symposium emphasized the urgency and opportunity in addressing muscle aging—a key driver of health and independence in older adults.
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Founded in 2008 by visionary scientists—Dr. Mikhail (Misha) Blagosklonny, Dr. Judith Campisi, and Dr. David Sinclair—Aging (Aging-US) was created as a platform for publishing innovative and sometimes unconventional ideas in the rapidly evolving field of aging. Supporting events like the MAST Symposium is not just aligned with this mission—it reflects our long-term commitment to advancing aging science and empowering the next generation of researchers.
“Breast cancer (BC) is the most commonly diagnosed cancer among women in the US and worldwide .”
Breast cancer survivors are living longer than ever, thanks to research and medical advances, but new studies suggest that some treatments may come with a hidden cost: accelerated aging. A recent study, titled “Accelerated aging associated with cancer characteristics and treatments among breast cancer survivors,” published inAging (Aging-US), reveals that breast cancer and its treatments may speed up biological aging, with effects lasting up to a decade post-diagnosis.
Breast Cancer and Aging
Breast cancer is one of the most common cancers among women worldwide. Medical advancements have dramatically improved survival rates, making it one of the most treatable forms of cancer. Yet, many survivors report lasting symptoms like fatigue, memory issues, and reduced vitality that resemble accelerated aging. This pattern has led scientists to investigate whether treatments for breast cancer might be contributing to biological age acceleration.
The Study: Measuring Long-Term Aging in Breast Cancer Patients
Researchers at Vanderbilt University conducted a decade-long study involving 1,264 breast cancer patients and 429 cancer-free women. The research team, led by first author Cong Wang and corresponding author Xiao-Ou Shu, used a tool called Phenotypic Age Acceleration (PAA), which estimates biological age using standard blood test data. Unlike chronological age, biological age reveals how “old” the body functions, offering a clearer picture of a person’s overall health and aging rate.
The Results: Long-Term Effects of Breast Cancer Treatments on Aging
At diagnosis, breast cancer patients already appeared nearly four years older biologically than their cancer-free counterparts. One year after treatment, they still seemed two years older. Even ten years later, signs of accelerated aging remained.
When it comes to treatments, not all had the same long-term impact on aging. Chemotherapy was linked to the most immediate spike in aging markers, with effects most noticeable in the first year. In contrast, endocrine therapy showed slower, long-term effects, becoming more apparent many years later. Surgery and radiation therapy were associated with lower levels of age acceleration over time, suggesting that localized treatments may carry fewer long-term aging effects than systemic therapies.
Tumor characteristics also influenced aging levels. Women diagnosed with advanced-stage cancer (Stage III or IV) or those with high-grade tumors experienced the most pronounced biological aging. These findings suggest that both the disease itself and the intensity of treatment contribute to how quickly a survivor may age.
The Breakthrough: Simple Blood Tests to Monitor Aging in Breast Cancer Survivors
This study provides valuable insight into how breast cancer and its treatments can impact survivors’ long-term health. One of its most important contributions is highlighting a simple, accessible way to track biological aging, the PAA test. This method is cost-effective, easy to use in regular medical care, and gives clinicians a powerful tool to identify high-risk patients and tailor long-term follow-up strategies.
The Impact: Rethinking Long-Term Breast Cancer Care
The paper offers valuable insights that could reshape how clinicians think about survivorship care. Breast cancer survivors already face increased risks for heart disease, osteoporosis, and cognitive decline. Accelerated aging may be a contributing factor. By identifying these effects early, healthcare providers can develop more personalized support strategies, potentially improving quality of life and long-term health outcomes.
Future Perspectives and Conclusion
The journey does not end with breast cancer remission. This study underscores that cancer and its treatments can leave lasting effects on the body’s aging process. Implementing appropriate strategies—whether medical, lifestyle-based, or a combination of both—may help survivors not only extend their lifespan but also increase their long-term health and quality of life.
Integrating biological age monitoring into routine follow-up care could enable healthcare providers to better understand each survivor’s health trajectory. For all the women navigating life after breast cancer, such information could translate into not just more years, but better years.
Click here to read the full research paper in Aging.
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Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed Central, Web of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).
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“This special collection will explore key themes central to Dr. Blagosklonny’s scientific contributions, with a focus on mechanistic insights, translational approaches, and theoretical perspectives.”
BUFFALO, NY — April 3, 2025 —Aging (Aging-US) is pleased to announce a special Call for Papers for a commemorative collection honoring the legacy of Dr. Mikhail (Misha) Blagosklonny, the founding editor of the journal and a pioneer in aging biology. His groundbreaking work shaped fundamental concepts in the field, particularly regarding the role of mTOR in aging and cancer, the use of rapamycin, bypassing senescence during the process of transformation, personalized medicine, and theories on why we age.
This special collection will explore key themes central to Dr. Blagosklonny’s scientific contributions, with a focus on mechanistic insights, translational approaches, and theoretical perspectives. We invite original research, reviews, and perspective articles covering topics such as:
The role of mTOR in aging and age-related diseases
Rapamycin and other pharmacological strategies to extend lifespan
Senescence bypass and its implications for cancer and regenerative medicine
Personalized medicine approaches in aging and longevity research
Theoretical models and evolutionary perspectives on aging
The special issue will be guest-edited by leading scientist in the field, David Gems, who will oversee the selection of high-quality contributions that reflect the depth and impact of Dr. Blagosklonny’s work.
We encourage researchers working on these topics to submit their manuscripts and contribute to this tribute to one of the most influential figures in aging research.
SUBMISSION DETAILS:
Submission Deadline: January 31, 2026 (UPDATED DEADLINE)
Alzheimer’s disease is a progressive neurological disorder that gradually steals memory, independence, and a person’s sense of identity. A defining feature of Alzheimer’s is the buildup of amyloid-β (Aβ) plaques—sticky protein clumps that interfere with communication between brain cells. This disruption is closely linked to changes in a group of enzymes called cholinesterases, especially acetylcholinesterase (AChE) and butyrylcholinesterase (BChE). These enzymes normally play a vital role in regulating neurotransmitters critical for memory, learning, and cognitive function. In Alzheimer’s, however, their behavior changes significantly, particularly when they interact with Aβ plaques.
The Study: Exploring Senolytics for Alzheimer’s Enzyme Inhibition
A research team from Dalhousie University in Canada looked into whether senolytic compounds—a class of drugs that eliminate damaged, aging cells often referred to as “zombie” cells—could also target the harmful forms of cholinesterase enzymes found in Alzheimer’s disease. Their goal was to see if these compounds could selectively inhibit the disease-associated versions of AChE and BChE, without affecting the healthy forms that are essential for normal brain function.
Led by Dr. Sultan Darvesh, the study tested six compounds: five senolytics—dasatinib, nintedanib, fisetin, quercetin, and GW2580—and one nootropic, meclofenoxate hydrochloride, known for its memory-enhancing potential. The researchers used post-mortem brain tissue from Alzheimer’s patients, enzyme activity assays, and computer modeling to examine how these compounds interact with the enzymes.
The Challenge: Targeting the Right Enzymes
One of the limitations of current Alzheimer’s treatments is that they do not distinguish between the normal and the altered forms of cholinesterases. While these drugs can raise levels of the memory-related chemical acetylcholine and improve cognitive function, they often come with side effects due to their broad activity. A more precise approach—targeting only the versions of AChE and BChE tied to Aβ plaques—could offer better outcomes with fewer drawbacks.
The Results: Senolytics Show Precision in Enzyme Targeting
The results were promising. Some of the senolytics tested, like dasatinib and nintedanib, effectively blocked the cholinesterases attached to Aβ plaques without affecting the normal versions of these enzymes in healthy brain tissue. Meclofenoxate also showed strong activity against the disease-associated forms. Interestingly, this selectivity was linked to how these compounds bind to the enzymes. Instead of locking onto the main active site, many of them attached to alternative regions, known as allosteric sites, which are only altered in the plaque-associated forms. This type of binding allowed the compounds to distinguish between harmful and healthy enzymes.
The Breakthrough: Targeting the Disease, Preserving the Brain
This study is the first to show that certain senolytic and cognitive-enhancing drugs can selectively inhibit the dysfunctional versions of cholinesterases found in Alzheimer’s without affecting their normal forms. This level of precision could mark a major step forward in Alzheimer’s therapy.
The Impact: A Dual-Action Path to Treating Alzheimer’s
By focusing on only the problematic forms of AChE and BChE, this approach could lead to Alzheimer’s treatments that better preserve cognitive function while avoiding side effects. The research also bridges two important areas of study: aging and neurodegeneration. It suggests that drugs developed to slow aging might also be used as targeted treatments for Alzheimer’s, offering a two-in-one therapeutic advantage.
Future Perspectives and Conclusion
Although more research is needed, especially in living models and clinical trials, the potential of the findings is encouraging. They lead the way for a new generation of Alzheimer’s treatments that are more targeted and safer.
By understanding better how aging and brain disease intersect at the cellular level, scientists may be moving closer to developing more effective and personalized approaches to combat Alzheimer’s.
Click here to read the full research paper in Aging.
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Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed Central, Web of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).
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“Epigenetic clocks can serve as pivotal biomarkers linking environmental exposures with biological aging.”
Could the air we breathe, the food we eat, or the chemicals in our everyday environment be accelerating our aging process? A recent study published in Aging suggests that exposure to certain environmental chemicals may be linked to faster biological aging through changes in DNA. These findings could have major implications for public health and longevity.
Understanding How Scientists Measure Aging at the DNA Level
Aging is not just about wrinkles and gray hair—it happens at the molecular level too. Scientists use epigenetic clocks to measure biological aging, which can differ from a person’s actual chronological age. These clocks track DNA methylation, a type of chemical modification that can change over time due to environmental factors like diet, pollution, and chemical exposure. Until now, there has been little research into how widespread environmental chemicals impact these aging markers.
The Study: Investigating the Impact of Environmental Pollutants on Aging
The Challenge: Unraveling the Complex Relationship Between Toxins and Aging
For years, scientists suspected that environmental toxins might contribute to aging, but most studies focused on a small set of chemicals. This work took a broader and more systematic approach to analyze a wide range of pollutants that people are commonly exposed to. The goal was to uncover previously unknown connections between chemical exposure and biological aging at the genetic level.
The Results: Environmental Chemicals That Speed Up Aging
The study identified several chemicals that were significantly associated with epigenetic age acceleration. One of the most concerning findings was the impact of cadmium, a toxic heavy metal found in cigarette smoke, industrial pollution, and some foods. Higher levels of cadmium in the blood were linked to faster aging across multiple epigenetic clocks.
Another key finding was the role of cotinine, a biomarker of tobacco exposure. People with higher levels of cotinine in their system showed signs of accelerated DNA aging, reinforcing the long-known link between smoking and premature aging.
The study also found that lead and dioxins, commonly found in industrial pollutants and certain processed foods, might contribute to biological aging. Interestingly, some pollutants, like certain polychlorinated biphenyls (PCBs), were associated with slower aging, though the health effects of these compounds remain unclear.
The Breakthrough: Why Cadmium and Smoking Are Major Aging Accelerators
This research highlights cadmium as a major environmental driver of aging. Since cadmium exposure comes from both smoking and diet, reducing it could be a key anti-aging strategy. The findings also provide further evidence that smoking is one of the most significant factors influencing epigenetic aging.
Reducing exposure to cigarette smoke, polluted air, and contaminated foods could help slow down DNA aging and potentially increase lifespan.
The Impact: How These Findings Can Influence Health Policies and Personal Choices
The results of this study could lead to stronger environmental regulations on heavy metals and toxic pollutants. Policymakers may push for stricter air quality standards, better food safety regulations, and more public health initiatives to reduce exposure to aging-accelerating chemicals.
For individuals, this research reinforces the importance of reducing exposure to toxins. Avoiding cigarette smoke, choosing organic and non-processed foods, and being mindful of products containing chemicals could help protect DNA health and promote longevity.
Future Perspectives and Conclusion
While this study provides strong evidence that environmental toxins influence aging, further research is needed to determine whether reducing exposure can slow down or even reverse epigenetic aging. Future studies could focus on younger populations and examine how lifestyle changes interact with these environmental exposures.
For now, taking steps to avoid cigarette smoke, limit exposure to heavy metals, and maintain a clean diet could be practical ways to protect long-term health and slow down biological aging.
By understanding how environmental pollutants impact aging, individuals and policymakers can make informed decisions that promote a longer, healthier life.
Click here to read the full research paper in Aging.
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Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed Central, Web of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).
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“These insights underscore the importance of personalized treatment approaches and the need for further research to improve radiotherapy outcomes in cancer patients.”
Radiation therapy or radiotherapy, is a common treatment for cancer, but its effectiveness differs across patients. A recent study published as the cover for Volume 17, Issue 2of Aging explored why this happens. The findings provide valuable insights, particularly for brain cancers like glioblastoma (GBM) and low-grade gliomas (LGG).
Understanding Glioblastoma and Low-Grade Gliomas
Glioblastoma and LGG are both brain tumors, but they behave in very different ways. GBM is highly aggressive, with most patients surviving only 12 to 18 months, even with surgery, chemotherapy, and radiation therapy. LGG, on the other hand, grows more slowly, and many patients live for decades with proper care.
The Study: Investigating Radiation Therapy’s Impact on Cancer Patients Survival
A research team led by first author Alexander Veviorskiy from Insilico Medicine AI Limited, Abu Dhabi, UAE, and corresponding author Morten Scheibye-Knudsen from the Center for Healthy Aging, University of Copenhagen, studied how radiation therapy affects cancer patient survival. They examined data from The Cancer Genome Atlas (TCGA), which includes 32 types of cancer. When they found that GBM and LGG had very different survival outcomes after radiation, they decided to focus on these two types of brain cancer. To learn more about their differences, gene expression and molecular pathways connected to radiation therapy responses were studied.
The Challenge: Why Radiation Therapy Works Only in Certain Tumors
Radiation therapy is an important cancer treatment, but its success is not the same for everyone. Even patients with the same type of cancer can respond differently, making it difficult to predict who will benefit. Understanding why some tumors are sensitive to radiation while others resist it is key to improving treatment and patient survival.
The Results: Radiation Therapy Works for Glioblastoma but Not for Low-Grade Gliomas
Overall, GBM had the highest percentage of patients receiving radiation therapy (82%), followed by LGG (54%). When researchers compared survival outcomes, they found that while radiation improved survival in breast cancer and GBM patients, it had a negative effect on patients with lung adenocarcinoma and LGG. This led researchers to take a closer look at GBM and LGG, especially since LGG can develop into GBM over time.
A key discovery was how GBM and LGG regulate DNA repair differently. GBM tumors have weak DNA repair activity, making them more vulnerable to radiation-induced damage. LGG tumors, however, activate more DNA repair pathways, allowing cancer cells to survive radiation and potentially making treatment less effective.
The immune response to radiation therapy was also different. In GBM, radiation triggered an immune response, which may help fight the tumor. In LGG, however, immune activation was significantly lower, meaning that radiation therapy did not enhance the body’s ability to attack cancer cells. This fact may contribute to worse survival outcomes for LGG patients after treatment.
Further genetic analysis revealed that ATRX gene mutations made GBM and LGG patients more sensitive to radiation. On the other hand, higher EGFR gene activity was linked to lower survival rates after radiation in LGG patients. Similar findings for GBM tumors indicate treatment resistance.
The Breakthrough: Toward Personalized Treatment
This study offers new insights into why radiation therapy benefits certain brain tumors while being less effective, particularly in GBM and LGG. Finding important biological factors, like DNA repair activity, immune response, and genetic changes that may serve as biomarkers, will help radiation therapy be more precisely tailored to each patient’s unique tumor profile.
The Impact: Rethinking Glioblastoma and Low-Grade Gliomas Treatment
These findings highlight the importance of precision medicine in brain cancer treatment. Instead of automatically recommending radiation therapy for all LGG patients, oncologists should consider genetic testing to determine whether this treatment will be beneficial or not. If not, alternative treatments may be necessary. Immunotherapy and targeted drugs against EGFR could provide better outcomes for patients who do not respond well to radiation therapy.
For GBM, researchers are investigating ways to enhance radiation’s effectiveness by combining it with DNA repair inhibitors, such as PARP inhibitors. These drugs could increase tumor sensitivity to radiation and improve survival rates.
Conclusion
Advancing cancer treatment requires a personalized approach. Identifying biomarkers that predict how GBM and LGG tumors respond to radiation therapy can help clinicians make more informed treatment decisions, ensuring that patients receive the most effective and least harmful therapies. By uncovering key genetic and molecular insights, this study moves the field closer to individualized brain cancer treatments, improving survival rates while reducing unnecessary risks for patients.
Click here to read the full research paper in Aging.
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Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed Central, Web of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).
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“Senescent cells accumulate in aging tissues, impairing their ability to undergo repair and regeneration following injury.”
Imagine a simple topical treatment that could help aging skin heal faster, reducing recovery time from wounds and even improving skin quality. Scientists may have found exactly that. A recent study, published in Aging, reveals that a compound called ABT-263 can eliminate aging cells in the skin, boosting its ability to regenerate.
Understanding How Aging Affects Skin Healing
Aging affects the skin’s structure and function, leading to a reduced ability to heal from wounds. Scientists have long suspected that senescent cells, also known as “zombie cells,” play a major role in this decline. These cells stop dividing but refuse to die, accumulating in tissues and releasing inflammatory molecules that impair the body’s natural repair processes.
Various studies have explored senolytics, a class of drugs designed to eliminate these aging cells and restore tissue function. While these drugs have shown promise in treating diseases like osteoporosis and fibrosis, their impact on skin regeneration and wound healing has been less studied. A new study titled “Topical ABT-263 treatment reduces aged skin senescence and improves subsequent wound healing” now suggests that a topical application of the senolytic ABT-263 could significantly improve wound healing in older individuals.
The Study: How Clearing Aging Cells Improves Skin Repair
A team of researchers from Boston University Aram V. Chobanian and Edward Avedisian School of Medicine, led by first author Maria Shvedova and corresponding author Daniel S. Roh, tested whether ABT-263 could enhance wound healing in aging skin. They applied topical ABT-263 to the skin of 24-month-old mice—roughly equivalent to elderly humans—over a five-day period. After the treatment period, the researchers created small skin wounds on the mice and monitored their healing process compared to a control group. They also analyzed molecular changes in the skin to understand how the drug influenced tissue repair.
The Challenge: Why Aging Skin Heals More Slowly
Older skin does not regenerate as well as younger skin due to a combination of factors. One key reason is the accumulation of senescent cells, which interfere with normal repair processes by increasing inflammation and reducing collagen production, a critical component of wound healing.
Even though the body has mechanisms to remove damaged cells, these processes weaken with age. As a result, senescent cells accumulate, contributing to chronic inflammation that delays wound closure.
The Results: Faster Healing and Improved Skin Function
The study found that topical ABT-263 effectively reduced the number of senescent cells in aged skin. Markers of cellular aging were significantly decreased, confirming that the drug successfully eliminated dysfunctional cells.
When wounds were induced after treatment, mice that received ABT-263 healed significantly faster than those in the control group. The researchers also observed an increase in gene activity related to collagen production, cell proliferation, and extracellular matrix organization—all crucial factors for effective wound repair.
Interestingly, the treatment triggered a temporary inflammatory response, with immune cells, particularly macrophages, infiltrating the treated skin at higher levels. This response, while short, appeared to accelerate repair by clearing out damaged tissue and promoting regeneration.
By day 15, the wounds of ABT-263-treated mice had closed significantly faster than those of untreated mice. By day 24, 80% of the treated mice had achieved complete wound closure, compared to only 56% in the control group.
The Breakthrough: A New Approach to Enhancing Skin Regeneration
This study provides strong evidence that removing senescent cells before an injury can prime aging skin for faster healing. The results suggest that topical senolytic drugs like ABT-263 could serve as a pre-treatment for surgeries or individuals prone to slow-healing wounds, providing a safer, more targeted approach than systemic treatments. Additionally, the observed increase in collagen expression suggests that this method not only accelerates healing but also improves the overall strength and quality of repaired skin.
The Impact on Wound Care and Skincare
If similar results can be achieved in humans, ABT-263 or similar senolytic treatments could become valuable tools, particularly for elderly patients undergoing surgery, where slow wound healing increases the risk of complications. It may also help individuals with chronic wounds, such as diabetic ulcers, which often struggle to heal properly. In post-surgical skincare, accelerating recovery could lead to better outcomes and reduced scarring. Additionally, in anti-aging dermatology, this treatment has the potential to reverse some of the cellular effects of aging on the skin.
Future Prospects and Conclusion
This study marks an important step toward clinical applications. While the findings are promising, further research is necessary to confirm whether ABT-263 offers similar benefits in humans. Clinical trials will be crucial in assessing its safety, efficacy, and long-term effects, particularly in wound healing and dermatological treatments. If successful, senolytic creams or topical therapies could offer new solutions for age-related skin challenges and slow-healing wounds.
Click here to read the full research paper in Aging.
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Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed Central, Web of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).
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“Brown adipose tissue (BAT), a major subtypes of adipose tissues, is known for thermogenesis and promoting healthful longevity.”
Emerging research suggests that a specific type of body fat may play an important role in healthy aging and physical performance. Researchers from Rutgers New Jersey Medical School explore this topic in a recent research perspective published in Aging (Aging-US). Their work discusses new findings and emerging ideas about the role of brown adipose tissue (BAT), commonly known as brown fat.
Understanding Brown Fat
The human body contains different types of fat. The most common is white adipose tissue (WAT), which primarily stores excess calories. When present in large amounts, WAT contributes to health problems like obesity, type 2 diabetes, and cardiovascular disease as a result of its role in metabolic imbalance.
In contrast, BAT serves a more dynamic role. Instead of storing energy, BAT burns calories to generate heat through a process called thermogenesis, powered by its high concentration of mitochondria—the energy-producing structures in cells. While BAT is abundant in newborns to help regulate body temperature, it persists in smaller amounts in adults, particularly around the neck, shoulders, and spine.
According to the research perspective, titled “Brown Adipose Tissue Enhances Exercise Performance and Healthful Longevity” brown fat’s role extends beyond thermoregulation. The authors suggest that BAT can significantly improve metabolic health, enhance physical performance, and promote healthful longevity.
How Brown Fat Enhances Physical Performance
While most studies focus on how exercise activates BAT, this research perspective suggests that brown fat itself may actively enhance physical performance. The authors, Dorothy E. Vatner, Jie Zhang, and Stephen F. Vatner, base their hypothesis on studies involving genetically modified mice lacking a protein called RGS14. These RGS14 knockout (KO) mice not only live longer but also exhibit improved endurance and better health markers compared to regular mice. These benefits are linked to the more active and efficient brown fat present in these genetically modified mice.
In experimental studies, brown fat from RGS14 knockout (KO) mice was transplanted into normal mice. The results were striking—within just three days, the recipient mice showed significant improvements in exercise performance, whereas mice that received brown fat from regular donors required several weeks to experience similar benefits.
These findings suggest that BAT is more than just a passive energy-burning tissue. It may actively influence strength, cardiovascular function, and overall health, highlighting BAT’s potential in supporting longevity.
The Importance of Brown Fat for Exercise and Aging
Different research studies highlight how BAT influences exercise capacity and aging. Beyond burning calories, BAT improves blood flow, enhances mitochondrial function, and reduces oxidative stress—factors essential for maintaining muscle health and endurance, especially with age.
In mice with active BAT, researchers observed increased blood vessel formation, which improves oxygen and nutrient delivery to muscles during physical activity. Combined with BAT’s support for mitochondrial health, this leads to greater stamina and resilience against age-related decline.
Additionally, BAT seems to offer broader health benefits, helping protect against conditions such as obesity, diabetes, heart disease, and neurodegenerative disorders like Alzheimer’s disease. All these findings highlight BAT’s potential, making it a possible target for therapies aimed at combating age-related conditions.
Future Directions: Brown Fat as a Potential Therapeutic Target
Various scientific findings about BAT have led researchers to suggest developing therapies that can mimic its effects. For example, a pharmaceutical analog of BAT could help treat age-related conditions, such as reduced physical capacity, metabolic disorders, and chronic diseases.
Beyond weight management, these therapies might enhance fitness, improve metabolic health, and support healthy aging, potentially extending lifespan. This approach could be especially valuable for individuals with limited mobility due to chronic conditions or age-related decline.
As research progresses, BAT-based therapies may transform how we address aging and metabolic diseases, offering new hope for improving quality of life.
Conclusion: Rethinking the Role of Brown Fat
Beyond its role in energy regulation, BAT may contribute to metabolic health, physical performance, and healthy aging.
Recognizing the potential health benefits of BAT challenges the traditional view of fat as something exclusively to reduce or eliminate. Instead, BAT appears to play an active role in the body’s metabolic processes, with potential implications for longevity and disease prevention. While further research is needed, exploring BAT’s functions may offer new strategies to support human health.
Click here to read the full research perspective in Aging.
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Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed Central, Web of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).
Click here to subscribe to Aging publication updates.
“We illustrate our strategy in brain and liver tissue, demonstrating how cell-type specific epigenetic clocks from these tissues can improve tissue-specific estimation of chronological and biological age.”
Aging affects everyone differently. There are two types of aging: chronological aging, which refers to the number of years a person has lived, and biological aging, which reflects how well the body is functioning based on cellular changes. A recent study published as the cover for Volume 16, Issue 22 of Aging reports a new discovery that could revolutionize the way we understand aging and its impact on health.
Understanding Biological Age
Biological age reflects how well the body is aging and can vary based on lifestyle, genetics, and environmental factors. Traditionally, scientists estimate it using epigenetic clocks, which measure DNA methylation, chemical changes that occur over time. Until recently, these clocks could only provide general estimates by analyzing entire tissues, meaning they could not distinguish how different cell types aged within those tissues. A recent study titled “Cell-type Specific Epigenetic Clocks to Quantify Biological Age at Cell-Type Resolution” aims to change that.
The Study: Measuring Aging More Precisely
To explore how different cell types age, researchers from the Chinese Academy of Sciences and Monash University analyzed publicly available DNA methylation data from brain and liver tissues using advanced computer models. The samples included healthy individuals and those with diseases like Alzheimer’s and non-alcoholic fatty liver disease.
In addition to brain and liver samples, the study included data from other tissues such as the prostate, colon, kidney, and skin. This broader dataset ensured that the findings applied to a wide range of conditions.
The Challenge: Understanding Aging at a Cellular Level
One of the biggest challenges in estimating biological age has been the inability to distinguish between different cell types within a tissue. Traditional methods analyze a tissue as a whole, averaging the age of all existing cells. This can hide the fact that some cells age faster than others, making it difficult to identify early signs of disease.
In organs like the brain and liver, different cell types—such as neurons and glial cells in the brain, or hepatocytes in the liver—age at different rates. Without a method to study cell types individually, it has been challenging to identifying which cells are most affected by aging and how they contribute to diseases like Alzheimer’s and liver diseases.
Aging is also influenced by two factors: intrinsic aging, which refers to changes within the cells themselves, and extrinsic aging, which occurs due to changes in cell composition within a tissue. Traditional methods struggle to separate these aspects, limiting their usefulness in developing targeted anti-aging treatments.
The Results: Key Findings in Alzheimer’s and Liver Disease
The study found that different types of cells within the same tissue age at different rates. In Alzheimer’s disease, neurons and glial cells in the brain showed signs of accelerated aging, with glial cells in the temporal lobe being the most affected. This suggests that glial cells could play a crucial role in the progression of neurodegeneration. Similarly, in liver conditions such as fatty liver disease and obesity, hepatocyte-specific clocks detected signs of accelerated aging that were not as easily identified previously.
By applying their approach to brain and liver tissues, the researchers demonstrated that cell-type specific epigenetic clocks can improve tissue-specific estimation of biological age, as well as chronological age.
The Breakthrough: Cell-Type Specific Epigenetic Clocks
Before this study, biological age could only be estimated at the tissue level, providing a general picture but not showing how individual cell types were changing over time. With the development of cell-type specific epigenetic clocks, researchers can now measure aging within specific types of cells, such as neurons in the brain and hepatocytes in the liver. Also, by distinguishing intrinsic aging from changes in cell composition, this new method offers new insights into how diseases develop and progress.
The Impact: What This Means for Healthcare
The implications of this research are significant. Measuring the biological age of individual cell types can lead to earlier diagnosis of age-related diseases, more effective treatments, and personalized healthcare plans. It could also help scientists track the effectiveness of anti-aging therapies and lifestyle changes more accurately, giving individuals better tools to manage their health.
This research also offers valuable insights into age-related conditions like Alzheimer’s and liver diseases, by pinpointing which cells experience the most stress and deterioration, allowing researchers to focus their efforts on the most affected cell types.
Future Prospects and Conclusion
Looking ahead, researchers plan to use this method to study other tissues and cell types, further advancing the field of precision medicine. As more data becomes available, cell-type specific epigenetic clocks could become essential tools for tracking aging at an individual level.
This study represents an exciting step forward in the science of aging. By measuring aging at the cellular level, scientists are moving closer to a future where aging can be better understood and managed.
Click here to read the full research paper in Aging.
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Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed Central, Web of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).
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