In this top-performing research perspective published by Aging on February 12, 2021, entitled, “DNA- and telomere-damage does not limit lifespan: evidence from rapamycin,” Dr. Mikhail Blagosklonny — an adjunct faculty member at Roswell Park Comprehensive Cancer Center and the Editor-in-Chief of Aging, Oncotarget, Oncoscience, and Cell Cycle — gleaned an important new perspective from recent aging studies, which some may have overlooked.

Rapamycin is a macrolide antibiotic that has immunosuppressive properties, regulates a key cellular growth pathway (mTOR), and has been at the center of numerous studies of aging since it’s discovery in 1964. Dr. Blagosklonny explains that, based on findings from recent mouse-model studies of rapamycin’s effects on short-lived mice, normal aging is not caused by the accumulation of molecular damage or telomere shortening.

“Here I discussed new evidence that normal aging is not caused by accumulation of molecular damage or telomere shortening: while extending normal lifespan in mice, rapamycin failed to do so in mice dying from molecular damage (Figure 1).”

To date, this research paper has generated an Altmetric Attention score of 43. Altmetric Attention scores, located at the top-left of trending Aging papers, provide an at-a-glance indication of the volume and type of online attention the research has received.

Top Aging publications rated by Altmetric score: https://www.aging-us.com/news_room/altmetric

DOI - https://doi.org/10.18632/aging.202674

Full text - https://www.aging-us.com/article/202674/text

Correspondence to: Mikhail V. Blagosklonny email: [email protected]

Keywords: quasi-programmed aging, hyperfunction theory, antagonistic pleiotropy, natural selection, mTOR, rapamycin

About Aging

Launched in 2009, Aging 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 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.

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