BUFFALO, NY — July 7, 2026 — A new #review was #published in Volume 18 of Aging on June 22, 2026, titled “The multifaceted inducers of cellular senescence.”

The review was led by first author Hilah Gal and corresponding author Valery Krizhanovsky from the Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.

Cellular senescence is a fundamental biological process in which damaged or stressed cells permanently stop dividing while remaining metabolically active. This response plays an essential role in suppressing tumor formation, supporting embryonic development, facilitating wound healing, and maintaining tissue integrity. However, as people age, senescent cells accumulate because they are no longer efficiently cleared by the immune system. Their persistence contributes to chronic inflammation, tissue dysfunction, cancer, and many age-related diseases.

In this comprehensive review, the authors examine the diverse biological stimuli that trigger cellular senescence and describe how seemingly different stimuli ultimately converge on common molecular pathways that establish stable growth arrest. Rather than viewing senescence as a single process, the review emphasizes its remarkable biological diversity and the importance of understanding how different initiating events shape distinct senescent cell phenotypes.

The review discusses several major biological inducers of cellular senescence. One of the best-established mechanisms is telomere attrition, in which repeated cell division gradually shortens chromosome ends until they trigger a persistent DNA damage response. Other important stimuli include direct DNA damage caused by ionizing radiation, ultraviolet light, chemotherapy, and oxidative injury, all of which activate cellular pathways that permanently halt proliferation.

Full press release - https://aging-us.net/2026/07/07/multiple-biological-triggers-shape-cellular-senescence-in-aging-and-disease/

DOI - https://doi.org/10.18632/aging.206391

Corresponding author - Valery Krizhanovsky - [email protected]

Abstract video - https://www.youtube.com/watch?v=5Y7R_8GQ1gk

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Keywords - aging, cell senescence

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As people live longer, maintaining good health is becoming just as important as extending lifespan. While chronological age simply reflects the number of years a person has lived, biological age measures how well the body is functioning and may better predict future health. Researchers have increasingly focused on lifestyle factors that may slow biological aging, and diet has emerged as one of the most promising.

A research paper published in Volume 18 of Aging titled “Plant-based dietary patterns are associated with slower epigenetic aging,” investigated whether diets emphasizing plant foods are associated with slower biological aging as measured by DNA methylation-based epigenetic clocks.

Full blog post - https://aging-us.org/2026/07/plant-based-dietary-patterns-are-associated-with-slower-biological-aging/

DOI - https://doi.org/10.18632/aging.206362

Corresponding author - Hyunju Kim - [email protected]

Abstract video - https://www.youtube.com/watch?v=FcJ7oEZ-KFk

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Keywords - aging, plant-based diets, DNA methylation, epigenetic aging, all-cause mortality, middle-aged adults

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BUFFALO, NY — July 6, 2026 — A new systematic #review was #published in Volume 18 of Aging on June 18, 2026, titled “Life expectancy and causes of death in classical laminopathic progeroid syndromes: systematic review with individual-patient data synthesis.”

The study was led by co-first authors Carlos López-Vila, Manuel García-Cordeiro, and Luís Estévez-Martínez from the University of Santiago de Compostela, and corresponding author David Araújo-Vilar from the University of Santiago de Compostela and the University Clinical Hospital of Santiago de Compostela, Spain.

Classical laminopathic progeroid syndromes are among the rarest inherited disorders known. Caused by mutations affecting the LMNA gene or the ZMPSTE24 enzyme, these conditions lead to premature aging, severe multisystem disease, and markedly shortened life expectancy. Although Hutchinson-Gilford progeria syndrome (HGPS), mandibuloacral dysplasia (MAD), and restrictive dermopathy (RD) all belong to this group, reliable information about survival and causes of death for each disorder has remained limited because most published reports describe only individual patients or small case series.

In this study, researchers performed a comprehensive systematic review and individual-patient data analysis to date of classical laminopathic progeroid syndromes. Following PRISMA guidelines, they analyzed data from 169 published studies together with two additional genetically confirmed institutional cases, creating a cohort of 158 genetically confirmed patients for the primary survival analysis. By examining individual patient records rather than pooled summaries, the investigators were able to compare survival patterns and causes of death across each disease subtype with greater precision.

Full press release - https://aging-us.net/2026/07/06/comprehensive-individual-patient-analysis-clarifies-life-expectancy-across-rare-progeria-disorders/

DOI - https://doi.org/10.18632/aging.206389

Corresponding author - David Araújo-Vilar - [email protected]

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Keywords - aging, progeria, Lamin A/C (LMNA), ZMPSTE24, survival, cause of death

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BUFFALO, NY — July 1, 2026 — A new #review was #published in Volume 18 of Aging on June 11, 2026, titled “Age-related dysfunctions of the neuroendocrine axes in nonhuman primates with depression-like and anxious behavior.”

The review, dedicated to the late Dr. Mikhail (Misha) Blagosklonny, was written by Nadezhda D. Goncharova from the Kurchatov Complex of Medical Primatology, National Research Center “Kurchatov Institute,” Adler, Sochi, Russian Federation.

As people grow older, their risk of developing stress-related disorders—including depression, metabolic disease, cardiovascular disease, cognitive decline, and neurodegenerative conditions—increases substantially. However, not everyone ages in the same way. Some individuals appear more resilient to stress, while others develop endocrine and metabolic disturbances that may accelerate aging and disease. Understanding the biological mechanisms behind these differences could help identify people at greater risk and support more personalized approaches to healthy aging.

In this review, the author summarizes decades of experimental research investigating how aging affects two major neuroendocrine systems—the hypothalamic-pituitary-adrenal (HPA) axis and the hypothalamic-pituitary-thyroid (HPT) axis—in nonhuman primates displaying either typical adaptive behavior or depression-like and anxiety-like behavior. Because rhesus monkeys closely resemble humans in their physiology, endocrine function, and behavior, they provide a valuable translational model for studying age-related changes that are difficult to examine in people.

The research shows that older monkeys with depression-like and anxiety-like behavior develop more pronounced dysfunction of the HPA axis than animals with standard behavior. These animals exhibited impaired negative feedback regulation, higher evening and nighttime cortisol levels, increased responses to acute stress, and greater activation of stress-related hormonal pathways. Together, these findings suggest impaired regulation of stress responses during aging.

The review also describes important age-related alterations in thyroid function. Older animals with depression-like and anxiety-like behavior showed lower thyroxine secretion, diminished thyroid responsiveness to hormonal stimulation, and evidence of impaired thyroid gland function. These endocrine changes were accompanied by greater insulin resistance, altered triglyceride metabolism, and reduced insulin secretion in overweight animals, indicating that stress-related neuroendocrine dysfunction may extend well beyond the brain.

Importantly, the findings suggest that behavioral characteristics may influence how endocrine systems age. Rather than experiencing identical biological changes over time, individuals with greater vulnerability to stress may develop more severe hormonal disturbances that contribute to age-related disease.

Full press - https://aging-us.net/2026/07/01/nonhuman-primate-research-reveals-how-aging-stress-and-behavior-may-interact-to-increase-disease-risk/

DOI - https://doi.org/10.18632/aging.206388

Corresponding author - Nadezhda D. Goncharova - [email protected] (ORCID id: 0000-0002-2720-9846)

Abstract video - https://www.youtube.com/watch?v=yj8zvthBiA4

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BUFFALO, NY — June 29, 2026 — A new #review was #published in Volume 18 of Aging on May 30, 2026, titled “The love and hate relationship between cellular senescence and stemness.”

The review was led by first author Angelos Papaspyropoulos and corresponding author Vassilis G. Gorgoulis from the National and Kapodistrian University of Athens and the Biomedical Research Foundation of the Academy of Athens, Greece.

Cellular senescence and stemness have traditionally been viewed as biological opposites. Senescent cells permanently stop dividing in response to cellular stress, helping prevent the spread of damaged cells, while stem cells maintain tissue repair by continuously renewing themselves and generating specialized cells. However, growing evidence suggests that the relationship between these two biological processes is far more complex and depends on the tissue type, physiological conditions, and disease context.

In this review, the authors summarize recent research examining how senescence and stemness interact across normal tissues, aging, regeneration, and cancer. Rather than always opposing one another, the two processes can either suppress or reinforce each other depending on the biological setting.

Under normal physiological conditions, senescence often limits stem cell activity. The review highlights studies showing that excessive senescence can impair the regenerative capacity of mesenchymal stem cells, muscle satellite cells, dental pulp stem cells, and pancreatic β-cell progenitors. In several experimental models, reducing senescence restored stem cell function and improved tissue regeneration.

At the molecular level, multiple signaling pathways contribute to this balance, including the p53/p21 and p16INK4A/RB pathways, mTOR signaling, Wnt/β-catenin signaling, and the senescence-associated secretory phenotype (SASP). These pathways help determine whether cells maintain regenerative potential or enter a stable senescent state.

The review also emphasizes that the relationship changes dramatically in cancer. In many tumors, senescent cells can promote the emergence of cancer stem cells through inflammatory signals released as part of the SASP or through cells escaping from the senescent state. This interaction has been reported in several malignancies, including B-cell lymphoma, liver cancer, colon cancer, lung cancer, and breast cancer, where stem cell-like properties may contribute to tumor progression, metastasis, and resistance to therapy.

Full press release - https://www.aging-us.com/news-room/cellular-senescence-and-stem-cells-share-a-more-complex-relationship-than-previously-recognized

DOI - https://doi.org/10.18632/aging.206387

Corresponding author - Vassilis G. Gorgoulis - [email protected]

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Keywords - aging, senescence, stemness

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BUFFALO, NY — June 25, 2026 — A new #research paper was #published in Volume 18 of Aging on May 29, 2026, titled “Short-term responsiveness of DNA methylation–based aging biomarkers to a multimodal intervention comprising exercise and dietary guidance involving daily consumption of yogurt containing Bifidobacterium longum BB536: an exploratory randomized controlled trial.”

The study, selected as our Editors’ Choice, was led by first author Tatsuki Nishimura and corresponding author Yukihiro Hishida from the R&D Division of Morinaga Milk Industry Co., Ltd., Japan.

As researchers continue searching for practical ways to promote healthy aging, increasing attention has focused on interventions that target multiple biological pathways simultaneously. While exercise and healthy eating are widely recognized as important components of healthy aging, scientists are also investigating whether specific dietary components and gut microbes may influence biological aging processes measurable at the molecular level.

In this study, researchers evaluated whether a 12-week lifestyle program could affect DNA methylation–based biomarkers of aging in overweight men aged 50 years and older. The intervention combined individualized exercise guidance, dietary counseling, and daily consumption of yogurt containing Bifidobacterium longum BB536, a probiotic strain that has previously been linked to beneficial effects on inflammation and gut health.

The randomized controlled trial enrolled 48 participants, who were assigned either to the intervention group or to a control group that maintained their usual lifestyle habits. Participants in the intervention group received dietary counseling focused on reducing overeating, exercise guidance encouraging regular walking or stepper-based activity, and a daily serving of yogurt containing Bifidobacterium longum BB536.

To assess biological aging, the investigators measured several DNA methylation–based aging biomarkers before and after the 12-week intervention. Particular attention was given to DunedinPACE, an epigenetic measure designed to estimate the current pace of biological aging rather than biological age itself.

Full press release - https://aging-us.net/2026/06/25/lifestyle-intervention-linked-to-slower-biological-aging-markers-in-older-men/

DOI - https://doi.org/10.18632/aging.206386

Corresponding author - Yukihiro Hishida - [email protected]

Abstract video - https://www.youtube.com/watch?v=7W5sDpGgZtE

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Keywords - aging, DNA methylation clock, DunedinPACE, Multicomponent lifestyle intervention, Bifidobacterium longum BB536

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BUFFALO, NY — June 23, 2026 — A new #research paper was #published in Volume 18 of Aging on May 28, 2026, titled “p38MAP kinase regulates senescence in human iPS-derived myocytes.”

The study was led by first author Hiroki Sato and corresponding author Ryuichiro Sato from The University of Tokyo, along with corresponding author Makoto Shimizu from The University of Tokyo and Ochanomizu University.

As people age, skeletal muscle gradually loses strength, mass, and function, contributing to frailty, reduced mobility, and an increased risk of falls. Although cellular senescence is widely recognized as a major driver of aging, the mechanisms that promote aging within mature muscle fibers remain poorly understood. In this study, researchers developed a human cell-based model to investigate how senescence develops in skeletal muscle cells and identified a signaling pathway that appears to play a central role in the process.

The research team used human induced pluripotent stem cell (iPSC)-derived myocytes, specialized muscle cells generated from stem cells. To mimic age-related cellular damage, the investigators exposed the cells to low-dose X-ray irradiation, which induced DNA damage without causing extensive cell death.

The treated muscle cells developed several characteristics commonly associated with aging. They exhibited muscle fiber atrophy, reduced contractile activity, and increased expression of p21, a well-established marker of cellular senescence. The researchers also observed elevated production of senescence-associated secretory phenotype (SASP) factors, inflammatory and extracellular signaling molecules that are commonly released by senescent cells.

To better understand the molecular changes involved, the investigators performed proteomic, transcriptomic, and functional analyses. These studies revealed activation of p38 mitogen-activated protein kinase (p38MAPK), a signaling pathway previously linked to cellular stress responses and aging in other tissues.

Further experiments demonstrated that inhibiting p38MAPK partially attenuated several senescence-associated features in the muscle cells. Treatment with p38MAPK inhibitors reduced muscle fiber atrophy, improved contractile function, and suppressed the expression of several senescence-associated factors. Conversely, activating p38MAPK promoted aging-like changes in the cells, further supporting its role in regulating muscle cell senescence.

The study also identified activation of an integrin–FAK/SRC–p38MAPK signaling axis following DNA damage. According to the authors, this pathway may help explain how cellular stress is translated into long-term functional decline in skeletal muscle.

Importantly, the findings were supported by analyses of human muscle aging datasets, which showed increased activity of MAPK signaling, focal adhesion pathways, and cytokine-related signaling in older skeletal muscle tissue.

Full press release - https://aging-us.net/2026/06/23/researchers-identify-key-signaling-pathway-driving-muscle-cell-aging/

DOI - https://doi.org/10.18632/aging.206385

Corresponding authors - Ryuichiro Sato - [email protected], and Makoto Shimizu - [email protected]

Abstract video - https://www.youtube.com/watch?v=ULm7R74CJx0

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As people live longer, maintaining mental well-being has become an increasingly important part of healthy aging. While regular physical activity is known to support both physical and psychological health, many older adults face barriers that make traditional exercise programs difficult to sustain. Researchers have therefore been exploring new approaches that combine physical activity with enjoyment, social interaction, and cognitive engagement.

A review published in Volume 18 of Aging titled “What are the effects of exergames on the mood states of older people? A systematic review of experimental studies, impacts on mental health and recommendations,” examined whether exergames—video games that require physical movement to play—can improve mood and mental health in older adults. The study was led by authors from the Laboratory of Sport and Exercise Psychology, Human Movement Sciences Graduate Program, College of Health and Sport Science of the Santa Catarina State University (UDESC) in Florianópolis, Brazil.

Full blog - https://aging-us.org/2026/06/do-exergames-improve-mood-and-mental-well-being-in-older-adults/

DOI - https://doi.org/10.18632/aging.206361

Corresponding author - Alexandro Andrade - [email protected]

Abstract video - https://www.youtube.com/watch?v=mNBh_alqVRI

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Keywords - aging, electronic games, older adults, BRUMS, mental health, physical activity

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BUFFALO, NY — June 18, 2026 — A new #research paper was #published in Volume 18 of Aging on May 26, 2026, titled “Early-life determinants of cardiometabolic outcomes and accelerated biological ageing in Colombia.”

The study was led by first and corresponding author Juan Carlos Rivillas from the Department of Epidemiology and Biostatistics, MRC Centre for Environment and Health, School of Public Health, Imperial College London, United Kingdom.

Experiences during childhood can shape health for decades. Adverse childhood experiences (ACEs), such as emotional abuse, domestic violence, food insecurity, poor health, and forced displacement, have long been linked to chronic disease. However, less is known about how these early-life hardships may influence biological aging itself. In this study, researchers examined whether childhood adversity is associated with cardiometabolic disease and accelerated biological aging among older adults in Colombia.

The investigators analyzed data from 3,385 adults aged 60 years and older who participated in the nationally representative SABE-Colombia study. Five forms of childhood adversity experienced before age 15 were evaluated: emotional abuse, domestic violence, poor childhood health, food scarcity, and forced migration related to Colombia’s armed conflict. Biological aging was estimated using the Klemera-Doubal Method for Biological Age, a biomarker-based measure that compares biological age with chronological age.

Full press release - https://aging-us.net/2026/06/18/childhood-adversity-may-leave-lasting-biological-scars-decades-later/

DOI - https://doi.org/10.18632/aging.206384

Corresponding author - Juan Carlos Rivillas - [email protected]

Abstract video - https://www.youtube.com/watch?v=5w6vgFzjcNQ

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Keywords - aging, adverse childhood experiences, forced childhood migration, biological ageing, cardiometabolic outcomes, life course epidemiology

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Each month, we will highlight a paper published in Aging chosen as the “Editors’ Choice.” These selections are handpicked by our editors and accompanied by a brief summary, showcasing research with significant impact and novel insights in aging and age-related diseases.

This exploratory randomized controlled trial, titled “Short-term responsiveness of DNA methylation–based aging biomarkers to a multimodal intervention comprising exercise and dietary guidance involving daily consumption of yogurt containing Bifidobacterium longum BB536: an exploratory randomized controlled trial,” investigated whether a 12-week lifestyle intervention combining exercise, dietary guidance, and daily consumption of yogurt containing Bifidobacterium longum BB536 could influence biological aging.

The researchers found a significant slowing of the DNA methylation-based pace of aging measure DunedinPACE in overweight men aged 50 and older, suggesting that feasible lifestyle changes may be associated with short-term improvements in selected epigenetic aging biomarkers.

DOI - https://doi.org/10.18632/aging.206386

Corresponding author - Yukihiro Hishida - [email protected]

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Keywords - aging, DNA methylation clock, DunedinPACE, Multicomponent lifestyle intervention, Bifidobacterium longum BB536

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