

Trending With Impact: Underlying Mechanisms of Replicative Senescence
Apr 26, 2022
06:54
Listen to a blog summary of a trending research paper selected as the cover for Volume 14, Issue 7 of Aging (Aging-US), entitled, "Downregulation of IGFBP5 contributes to replicative senescence via ERK2 activation in mouse embryonic fibroblasts."
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In 1961, Leonard Hayflick and Paul Moorhead proposed a theory later named the Hayflick Limit. They discovered that a normal human cell can divide between 50 and 70 times before it can no longer proliferate and eventually dies. Researchers have since continued to explore this phenomenon and, today, this aging process is known as cellular (replicative) senescence.
“There are currently several experimental models of cellular senescence. Hayflick and Moorhead observed that primary human fibroblasts in culture exhibit a limited proliferative capacity [6]. This growth arrest during passages is called replicative senescence.”
This permanent cessation of the cell cycle is universally found in biology due to known and unknown causes, including the shortening of telomeres. While telomere shortening plays an important role, it is not the only event responsible for inducing cellular senescence. Thus, researchers have spent decades under the microscope experimenting with cellular models of replicative senescence.
In a new study released on April 4, 2022, researchers from Sapporo Medical University in Sapporo, Japan, investigated mechanisms of replicative senescence in vitro. Their research paper was published on the cover of Aging (Aging-US) Volume 14, Issue 7, and entitled, “Downregulation of IGFBP5 contributes to replicative senescence via ERK2 activation in mouse embryonic fibroblasts.”
Full blog - https://aging-us.org/2022/04/trending-with-impact-underlying-mechanisms-of-replicative-senescence/
DOI - https://doi.org/10.18632/aging.203999
Corresponding author - Atsushi Kuno - kuno@sapmed.ac.jp
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Keywords - aging, IGFBP5, replicative senescence, mouse embryonic fibroblasts, ERK2, ERK1
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.
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