BUFFALO, NY- November 30, 2023 – A new #researchpaper was #published on the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 22, entitled, “Chronological aging impacts abundance, function and microRNA content of extracellular vesicles produced by human epidermal keratinocytes.”

The disturbance of intercellular communication is one of the hallmarks of aging. In their new study, researchers Taku Nedachi, Christelle Bonod, Julie Rorteau, Wafae Chinoune, Yuri Ishiuchi, Sandrine Hughes, Benjamin Gillet, Nicolas Bechetoille, Dominique Sigaudo-Roussel, and Jérôme Lamartine from the University of Lyon, Toyo University and Gattefossé SAS aimed to clarify the impact of chronological aging on extracellular vesicles (EVs), a key mode of communication in mammalian tissues. 

“The present study was therefore conducted to elucidate whether the characteristics of EVs released from cultured human keratinocytes can be modulated during aging process.”

The researchers focused on epidermal keratinocytes, the main cells of the outer protective layer of the skin which is strongly impaired in the skin of elderly. EVs were purified from conditioned medium of primary keratinocytes isolated from infant or aged adult skin. A significant increase of the relative number of EVs released from aged keratinocytes was observed whereas their size distribution was not modified.

By small RNA sequencing, the researchers described a specific microRNA (miRNA) signature of aged EVs with an increase abundance of miR-30a, a key regulator of barrier function in human epidermis. EVs from aged keratinocytes were found to be able to reduce the proliferation of young keratinocytes, to impact their organogenesis properties in a reconstructed epidermis model and to slow down the early steps of skin wound healing in mice, three features observed in aged epidermis. This work reveals that intercellular communication mediated by EVs is modulated during aging process in keratinocytes and might be involved in the functional defects observed in aged skin.

“To conclude, we have shown here that aging modulates EVs abundance, function and microRNA content in human keratinocytes.”
DOI - https://doi.org/10.18632/aging.205245

Corresponding author - Jérôme Lamartine - jerome.lamartine@univ-lyon1.fr

Sign up for free Altmetric alerts about this article - 
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205245

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

Keywords - aging, keratinocytes, microRNA, senescence, exosomes

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

Please visit our website at https://www.Aging-US.com​​ and connect with us:

SoundCloud - https://soundcloud.com/Aging-Us
Facebook - https://www.facebook.com/AgingUS/
X - https://twitter.com/AgingJrnl
Instagram - https://www.instagram.com/agingjrnl/
YouTube - https://www.youtube.com/@AgingJournal
LinkedIn - https://www.linkedin.com/company/aging/
Pinterest - https://www.pinterest.com/AgingUS/

Media Contact
18009220957
MEDIA@IMPACTJOURNALS.COM

Aging (Aging-US)

Aging Modulates Extracellular Vesicles of Epidermal Keratinocytes

BUFFALO, NY — March 3, 2026 — A new #research perspective was #published in Volume 18 of Aging-US on February 24, 2026, titled “A decline in glycolytic ATP production is the fundamental mechanism limiting lifespan; species with an optimal rate of decline over time survived.”

Led by Akihiko Taguchi — who is also the corresponding author and is affiliated with the Department of Regenerative Medicine Research, Foundation for Biomedical Research and Innovation at Kobe — the perspective advances a unifying conceptual framework in which a programmed or selected decline in glycolytic ATP production over the lifespan underlies aging phenotypes across species. The authors argue that glycolysis supplies the rapid ATP required for cell division and DNA/mitochondrial repair, and that a progressive reduction in glycolytic ATP with age can explain reduced cell proliferation, impaired repair, and other hallmark features of aging. 

“The simple explanation is that only species that happened to have an optimal rate of reduction in glycolytic ATP production over time were selected and survived through generational changes.”

The perspective synthesizes evidence from comparative biology, cellular metabolism, and translational studies to link glycolytic decline with lifespan variation among species — for example, contrasting short-lived rodents with long-lived species such as the naked mole rat, which maintain high glycolytic flux in low-oxygen niches. The authors also highlight mechanisms connecting glycolysis to mitophagy, telomere dynamics, and proteostasis, arguing that maintaining glycolytic ATP supports repair processes while a shift toward oxidative metabolism improves energy efficiency under resource limitation but reduces rapid-repair capacity.

The authors propose several concrete next steps to test the hypothesis. These include in vivo and in vitro interventions that modulate glycolysis (for example, gene transfer of glycolysis-related enzymes or pharmacologic activators such as terazosin), longitudinal measurements of glycolytic ATP production across aging cohorts, and comparative studies across species with differing lifespans to define the “optimal rate” of decline. They also suggest mechanistic studies of gap-junction–mediated metabolic coupling (for example, between hematopoietic stem cells and endothelium) and experiments to determine whether restoring glycolytic flux can rescue age-related deficits in DNA repair and tissue regeneration.

While the perspective offers a coherent conceptual model, the authors are explicit about limitations and caution: the idea is currently a hypothesis that requires experimental validation, and the evolutionary rationale (selection for an optimal rate of glycolytic decline) must be tested by comparative and mechanistic work. Translation to human rejuvenation therapies — whether via stem-cell approaches, metabolic activators, or gene transfer — will require careful preclinical studies to evaluate efficacy, safety, and long-term consequences.

DOI - https://doi.org/10.18632/aging.206356

Corresponding author - Akihiko Taguchi - taguchi@fbri.org

Abstract video - https://www.youtube.com/watch?v=rA23radaoqI

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at:

Bluesky - https://bsky.app/profile/aging-us.bsky.social
ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589
X - https://twitter.com/AgingJrnl
Facebook - https://www.facebook.com/AgingUS/
Instagram - https://www.instagram.com/agingjrnl/
LinkedIn - https://www.linkedin.com/company/aging/
Reddit - https://www.reddit.com/user/AgingUS/
Pinterest - https://www.pinterest.com/AgingUS/
YouTube - https://www.youtube.com/@Aging-US
Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc

MEDIA@IMPACTJOURNALS.COM

Aging-US

Next-Generation Metabolic Theory Suggests Glycolytic ATP Decline May Limit Lifespan

Aging reshapes the immune system in two fundamental ways: it alters the proportions of different immune cell types circulating in the blood, and it induces molecular changes within each individual cell. For years, researchers have struggled to disentangle these two intertwined processes using standard “bulk” measurements, which average signals across millions of cells and obscure what is happening at the single-cell level.

A new research paper, titled “Single-cell transcriptomics reveal intrinsic and systemic T cell aging in COVID-19 and HIV” published in Volume 18 of Aging-US by researchers at the Buck Institute for Research on Aging in California, the University of Southern California, and the University of Copenhagen, introduces an innovative solution. 

The team of Alan Tomusiak, Sierra Lore, Morten Scheibye-Knudsen, and corresponding author Eric Verdin, developed a novel tool called Tictock (T immune cell transcriptomic clock) that uses single-cell RNA sequencing to separately measure systemic and cell-intrinsic components of immune aging, and then applied it to understand how COVID-19 and HIV affect T cells.

Full blog - https://aging-us.org/2026/03/tictock-a-single-cell-clock-measures-immune-aging-in-viral-infections/

Paper DOI - https://doi.org/10.18632/aging.206353

Corresponding author - Eric Verdin - EVerdin@buckinstitute.org

Abstract video - https://www.youtube.com/watch?v=_r3AF7OrgKY

Sign up for free Altmetric alerts about this article - 
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206353

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

Keywords - aging, transcriptomic clock, aging biomarkers, systemic aging, intrinsic aging

To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at:

Bluesky - https://bsky.app/profile/aging-us.bsky.social
ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589
X - https://twitter.com/AgingJrnl
Facebook - https://www.facebook.com/AgingUS/
Instagram - https://www.instagram.com/agingjrnl/
LinkedIn - https://www.linkedin.com/company/aging/
Reddit - https://www.reddit.com/user/AgingUS/
Pinterest - https://www.pinterest.com/AgingUS/
YouTube - https://www.youtube.com/@Aging-US
Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc

MEDIA@IMPACTJOURNALS.COM

Tictock: A Single-Cell Clock Measures Immune Aging in Viral Infections

Biomarkers of aging help researchers understand how diseases influence the body over time. However, most current biomarkers rely on measurements from mixed cell populations, making it difficult to distinguish between changes caused by shifts in cell types and aging processes occurring within individual cells.

In this study, titled “Single-cell transcriptomics reveal intrinsic and systemic T cell aging in COVID-19 and HIV” and published in Volume 18 of Aging-US, researchers used single-cell RNA sequencing to analyze aging-related changes in human T cells. They developed Tictock, a single-cell transcriptomic clock that predicts both cellular age and T cell type across six human T cell subsets.

Applying this tool, the researchers found that acute COVID-19 was associated with increased proportions of CD8⁺ cytotoxic T cells, while T cell composition remained relatively stable in individuals with HIV receiving antiretroviral therapy (HIV+ART). Despite these differences, both conditions showed signs of accelerated transcriptomic aging, particularly in naïve CD8⁺ T cells.

Further analysis identified shared aging-related genes and biological pathways linked to ribosomal components and TNF receptor binding. These findings demonstrate how single-cell transcriptomic biomarkers can help separate systemic immune changes from cell-intrinsic aging processes, providing new tools to measure immune aging in disease.

DOI - https://doi.org/10.18632/aging.206353

Corresponding author - Eric Verdin - EVerdin@buckinstitute.org

Abstract video - https://www.youtube.com/watch?v=_r3AF7OrgKY

Sign up for free Altmetric alerts about this article - 
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206353

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

Keywords - aging, transcriptomic clock, aging biomarkers, systemic aging, intrinsic aging

To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at:

Bluesky - https://bsky.app/profile/aging-us.bsky.social
ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589
X - https://twitter.com/AgingJrnl
Facebook - https://www.facebook.com/AgingUS/
Instagram - https://www.instagram.com/agingjrnl/
LinkedIn - https://www.linkedin.com/company/aging/
Reddit - https://www.reddit.com/user/AgingUS/
Pinterest - https://www.pinterest.com/AgingUS/
YouTube - https://www.youtube.com/@Aging-US
Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc

MEDIA@IMPACTJOURNALS.COM

Aging-US Editors' Choice (March, 2026)

BUFFALO, NY — March 10, 2026 — A new #research paper was #published in Volume 18 of Aging-US on March 3, 2026, titled “P38 MAPK is involved in epigenetic regulation of fibrotic genes in replication induced senescence in lung fibroblasts.”

Led by Shan Zhu — with corresponding author Yan Y Sanders from the Department of Biomedical and Translational Sciences, Eastern Virginia Medical School (Macon & Joan Brock Virginia Health Sciences at Old Dominion University) — the study examines how the stress-activated kinase p38 MAPK contributes to persistent profibrotic gene expression in replicative (passage-driven) senescence of human lung fibroblasts and in primary fibroblasts from patients with idiopathic pulmonary fibrosis (IPF). 

Using IMR90 lung fibroblasts at low and high population-doubling levels and primary IPF fibroblasts, the authors show that TGF-β1 upregulates profibrotic genes (α-SMA and Col3A1) in both young and near-senescent cells, but that high-PDL (near-senescent/senescent) fibroblasts exhibit a delayed but sustained p38 MAPK response to TGF-β1. Pharmacological inhibition of p38 MAPK (SB202190) blunted profibrotic transcription and reduced H4K16 acetylation (H4K16ac) enrichment at α-SMA and Col3A1 promoters, indicating an epigenetic mechanism linking p38 signaling to fibrotic gene activation. 

“These findings suggest that a p38 MAPK–dependent epigenetic mechanism is involved in fibroblast activation, supporting the therapeutic potential of p38 MAPK inhibition for treating age-related fibrotic diseases such as IPF.”

The authors place these molecular results in a clinical context: persistent fibroblast activation and senescence are features of IPF and other age-associated fibrotic disorders, and the data here support targeting p38 MAPK to interrupt an epigenetically reinforced profibrotic program. The study used multiple readouts (western blot, RT-qPCR, ChIP for H4K16ac) and included primary IPF cells to strengthen translational relevance, while also noting that further work is required to test safety and efficacy in vivo.

The paper outlines clear next steps: determine the upstream triggers that sustain p38 signaling in near-senescent fibroblasts, map the chromatin-level events downstream of p38 that maintain H4K16ac at profibrotic promoters, and evaluate p38 inhibition in animal models of age-related pulmonary fibrosis. The authors also recommend exploring whether epigenetic modulators that reverse H4K16ac enrichment can synergize with kinase inhibition to restore repair capacity without impairing normal tissue healing.

DOI - https://doi.org/10.18632/aging.206357

Corresponding author - Yan Y Sanders - sandery@odu.edu

Abstract video - https://www.youtube.com/watch?v=yP0CwWMUhnY

Sign up for free Altmetric alerts about this article - 
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206357

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

Keywords - aging, senescence, fibroblast activation, p38 MAPK, lung fibrosis, H4K16Ac

To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at:

Bluesky - https://bsky.app/profile/aging-us.bsky.social
ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589
X - https://twitter.com/AgingJrnl
Facebook - https://www.facebook.com/AgingUS/
Instagram - https://www.instagram.com/agingjrnl/
LinkedIn - https://www.linkedin.com/company/aging/
Reddit - https://www.reddit.com/user/AgingUS/
Pinterest - https://www.pinterest.com/AgingUS/
YouTube - https://www.youtube.com/@Aging-US
Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc

MEDIA@IMPACTJOURNALS.COM

P38 MAPK Linked to Epigenetic Activation of Fibrotic Genes in Senescent Lung Fibroblasts

Cancer treatment has long been a battle of attrition—surgery, radiation, and chemotherapy have saved countless lives, but for patients with advanced or refractory malignancies, the options remain limited. In recent years, however, a new approach has emerged that harnesses the power of the patient’s own immune system to seek and destroy cancer cells with unprecedented precision.

An editorial perspective, titled “CAR-T therapy: Trailblazing CAR(ing) in cancer treatment.” published in Volume 17 of Oncotarget by researchers Uzma Saqib, Monika Pandey, and Krishnan Hajela from the School of Life Sciences, Devi Ahilya Vishwavidyalaya, Indore, India, provides an overview of this revolutionary therapeutic strategy. The paper presents the current state of CAR-T therapy, its clinical successes, and the formidable challenges that remain before it can fulfill its transformative potential.

Full blog - https://www.oncotarget.org/2026/03/10/car-t-cell-therapy-a-revolutionary-approach-to-cancer-treatment/

Paper DOI - https://doi.org/10.18632/oncotarget.28836

Correspondence to - Krishnan Hajela - hajelak@gmail.com

Abstract video - https://www.youtube.com/watch?v=T4hbwPToVKI

Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28836

Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/

Keywords - cancer, CAR-T therapy, therapeutic approaches

To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us:

Facebook - https://www.facebook.com/Oncotarget/
X - https://twitter.com/oncotarget
Instagram - https://www.instagram.com/oncotargetjrnl/
YouTube - https://www.youtube.com/@OncotargetJournal
LinkedIn - https://www.linkedin.com/company/oncotarget
Pinterest - https://www.pinterest.com/oncotarget/
Reddit - https://www.reddit.com/user/Oncotarget/
Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh

MEDIA@IMPACTJOURNALS.COM

Oncotarget

CAR-T Cell Therapy: A Revolutionary Approach to Cancer Treatment

BUFFALO, NY — March 13, 2026 — A new #research paper was #published in Volume 18 of Aging-US on March 2, 2026, titled “D, L-Buthionine-(S, R)-sulfoximine recapitulates the anti-obesity effects of sulfur amino acid restriction without the associated deleterious effects on bone in male mice.”

Led by Naidu B. Ommi from the Orentreich Foundation for the Advancement of Science — with corresponding author Sailendra N. Nichenametla from the same institution — the study tests whether the glutathione (GSH)-lowering compound D, L-buthionine-(S, R)-sulfoximine (BSO) reproduces the anti-obesity effects of sulfur amino acid restriction (SAAR) without causing the bone loss seen with SAAR diets. Using diet-induced obese male C57BL6/NTac mice fed high-fat diets, the authors compared: a control methionine-replete diet, a SAAR diet (low methionine, no cysteine), SAAR plus the GSH precursor N-acetylcysteine (NAC), and control diet plus BSO in drinking water. 

Using body-composition, micro-CT, histomorphometry, and biomechanical testing, the team confirmed prior work that SAAR reduces body fat but also lowers trabecular and cortical bone mineral density, increases marrow adiposity, reduces osteoblast numbers, and weakens bone biomechanical strength. Crucially, while NAC supplementation reversed the bone defects of SAAR (implicating cysteine/glutathione restriction in bone loss), BSO reproduced the lean, anti-obesity phenotype without producing the deleterious bone effects observed in SAAR mice. In short, BSO recapitulated the anti-obesity benefits of SAAR without causing the same bone loss — a finding with potential relevance to developing anti-obesity strategies that avoid skeletal harm.

“Despite its anti-obesity effects, BSO did not exert any detrimental effects on bones.”

The authors emphasize next steps and caveats. They call for mechanistic studies to define how GSH lowering drives fat loss yet spares bone under BSO treatment, investigations of age-at-onset, tissue-specific, and sex-specific effects, and long-term safety studies to assess off-target or delayed adverse effects of BSO before any clinical development. The paper frames BSO as a promising tool compound to dissect the beneficial versus deleterious axes of sulfur amino acid biology, but not yet as a human therapy without further preclinical evaluation.

DOI - https://doi.org/10.18632/aging.206358

Corresponding author - Sailendra N. Nichenametla - snichenametla@orentreich.org

Abstract video - https://www.youtube.com/watch?v=0adFA_b-q1Q

Sign up for free Altmetric alerts about this article - 
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206358

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

Keywords - bone, aging, methionine, glutathione, redox

To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at:

Bluesky - https://bsky.app/profile/aging-us.bsky.social
ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589
X - https://twitter.com/AgingJrnl
Facebook - https://www.facebook.com/AgingUS/
Instagram - https://www.instagram.com/agingjrnl/
LinkedIn - https://www.linkedin.com/company/aging/
Reddit - https://www.reddit.com/user/AgingUS/
Pinterest - https://www.pinterest.com/AgingUS/
YouTube - https://www.youtube.com/@Aging-US
Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc

MEDIA@IMPACTJOURNALS.COM

BSO Recapitulates Anti-Obesity Effects of Sulfur Amino Acid Restriction Without Bone Loss

BUFFALO, NY – March 16, 2025 – Impact Journals (publisher of Aging-US, Oncotarget, Oncoscience, and Genes & Cancer), is pleased to announce its participation as an exhibitor at the American Association for Cancer Research (AACR) Annual Meeting 2026. The meeting will take place April 17–22, 2026, at the San Diego Convention Center in San Diego, CA.

Conference attendees are warmly invited to visit Booth 3641 to meet members of the Impact Journals team, discover notable recent publications, and discuss opportunities for collaboration.

The mission of Impact Journals is to maximize research impact through insightful peer review, eliminate borders between specialties by linking different fields of oncology and biomedical science, and foster the application of both basic and clinical science. This mission is grounded in a strong commitment to ethical standards and scientific integrity. At Impact Journals, evolving digital technologies, tools, and ideas are continually integrated into a robust scientific integrity process.

The AACR Annual Meeting serves as a focal point for the global cancer research community, bringing together scientists, clinicians, healthcare professionals, survivors, patients, and advocates to share the latest advances in cancer science and medicine. From population science and prevention to cancer biology, translational and clinical studies, survivorship, and advocacy, the AACR Annual Meeting highlights the work of leading researchers from institutions around the world.

To learn more about Impact Journals, please visit impactjournals.com.

For media inquiries, email media@impactjournals.com.

Impact Journals to Participate at AACR Annual Meeting 2026 in San Diego

The aging of an organism is reflected not only in the function of its organs but also in the molecular signatures written into its cells. For years, scientists have cataloged the changes in protein-coding genes and various non-coding RNAs that occur as we grow older. However, one class of molecules—circular RNAs originating from the genome of our cellular power plants, the mitochondria—has remained largely unexplored.

A new research paper, titled “Aging-associated mitochondrial circular RNAs” published in Volume 18 of Aging-US by a multi-institutional team of researchers, provides the first detailed profile of these molecules and reveals a surprising link to cellular energy metabolism. 

The team’s investigation demonstrates that a specific mitochondrial circular RNA, circMT-RNR2, is depleted in older individuals and plays a direct role in regulating the TCA cycle, the engine of cellular energy production.

Full blog - https://aging-us.org/2026/03/mitochondrial-circular-rnas-new-players-in-human-aging/

Paper DOI - https://doi.org/10.18632/aging.206354

Corresponding authors - Je-Hyun Yoon - jehyun-yoon@ou.edu, and Young-Kook Kim - ykk@jnu.ac.kr

Abstract video - https://www.youtube.com/watch?v=f8uZ6_tcOHw

Sign up for free Altmetric alerts about this article - 
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206354

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

Keywords - aging, circular RNA, MT-RNR2, GRSF1, TCA cycle

To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at:

Bluesky - https://bsky.app/profile/aging-us.bsky.social
ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589
X - https://twitter.com/AgingJrnl
Facebook - https://www.facebook.com/AgingUS/
Instagram - https://www.instagram.com/agingjrnl/
LinkedIn - https://www.linkedin.com/company/aging/
Reddit - https://www.reddit.com/user/AgingUS/
Pinterest - https://www.pinterest.com/AgingUS/
YouTube - https://www.youtube.com/@Aging-US
Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc

MEDIA@IMPACTJOURNALS.COM

Mitochondrial Circular RNAs: New Players in Human Aging

BUFFALO, NY — March 18, 2026 — A new #editorial was #published in Volume 18 of Aging-US on March 10, 2026, titled “Healthy life extension: Geroscience’s north star.”

Led by David A. Barzilai — who is affiliated with Geneva College of Longevity Science, Healthspan Coaching LLC (Barzilai Longevity Consulting), and Harvard Medical School — the editorial pays tribute to the late Mikhail Blagosklonny and states that geroscience should adopt healthy life extension (measured as health-adjusted survival such as HALE and QALYs) as its primary objective rather than treating lifespan and healthspan as competing goals. Dr. Barzilai urges clearer outcome priorities, disciplined evidence in mammals, and coordinated investment that matches the field’s potential to delay multimorbidity and extend high-quality years of life.

The piece reviews data showing that increases in life expectancy have outpaced gains in healthy life expectancy and summarizes calls to measure success by health-adjusted longevity rather than biomarkers alone. It highlights examples where targeting conserved aging pathways produced replicable lifespan gains in mammals (for example, rapamycin in mice) and notes early human-facing signals (for example, mTOR inhibition improving influenza vaccine responses in older adults) that illustrate how aging-biology interventions can be clinically legible on shorter timelines. The editorial also frames the practical challenge: while lifespan evidence is ideal, human trials must use rigorous, meaningful endpoints that map to delayed multimorbidity, preserved function, and resilience. 

“Geroscience is for healthy life extension. We should stop pretending that lifespan and healthspan compete.”

Dr. Barzilai calls for a “moonshot”-level commitment to aging biology that includes larger, better-funded basic programs, clinical trials with health-adjusted survival endpoints, and translational pipelines able to move robust mammalian lifespan findings toward human studies. He stresses the need for replicable mammalian lifespan data paired with human endpoints that reflect quality of life and independence. The editorial closes with a direct pledge in honor of Dr. Blagosklonny’s legacy, in part to make healthy life extension the field’s north star and measure success in years worth living.

DOI - https://doi.org/10.18632/aging.206359

Corresponding author - David A. Barzilai - d.barzilai@gcls.study

Intro video - https://www.youtube.com/watch?v=_MwFvDg7Ejw

Sign up for free Altmetric alerts about this article - 
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206359

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

Keywords - aging, geroscience, longevity, healthspan, longevity medicine, healthy life extension

To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at:

Bluesky - https://bsky.app/profile/aging-us.bsky.social
ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589
X - https://twitter.com/AgingJrnl
Facebook - https://www.facebook.com/AgingUS/
Instagram - https://www.instagram.com/agingjrnl/
LinkedIn - https://www.linkedin.com/company/aging/
Reddit - https://www.reddit.com/user/AgingUS/
Pinterest - https://www.pinterest.com/AgingUS/
YouTube - https://www.youtube.com/@Aging-US
Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc

MEDIA@IMPACTJOURNALS.COM

Healthy Life Extension Positioned as Geroscience’s North Star

Aging-US is dedicated to advancing our understanding of the biological mechanisms that drive aging and the development of age-related diseases. Our mission is to serve as a platform for high-quality research that uncovers the cellular, molecular, and systemic processes underlying aging, and translates these insights into strategies to extend healthspan and delay the onset of chronic disease.

Read about the Aging-US Scientific Integrity Process: https://aging-us.com/scientific-integrity

Aging Modulates Extracellular Vesicles of Epidermal Keratinocytes

Aging-US Podcast

Related tracks