Open AccessMYSM1 Suppresses Cellular Senescence and the Aging Process to Prolong Lifespan
Author(s) -
Tian Mingfu,
Huang Yuqing,
Song Yunting,
Li Wen,
Zhao Peiyi,
Liu Weiyong,
Wu Kailang,
Wu Jianguo
Publication year - 2020
Publication title -
advanced science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.388
H-Index - 100
ISSN - 2198-3844
DOI - 10.1002/advs.202001950
Subject(s) - senescence , cellular senescence , process (computing) , suppressor , cellular aging , healthy aging , longevity , microbiology and biotechnology , accelerated aging , biology , telomere , gerontology , medicine , dna , phenotype , gene , chemistry , genetics , computer science , operating system
Aging is a universal feature of life that is a major focus of scientific research and a risk factor in many diseases. A comprehensive understanding of the cellular and molecular mechanisms of aging are critical to the prevention of diseases associated with the aging process. Here, it is shown that MYSM1 is a key suppressor of aging and aging‐related pathologies. MYSM1 functionally represses cellular senescence and the aging process in human and mice primary cells and in mice organs. MYSM1 mechanistically attenuates the aging process by promoting DNA repair processes. Remarkably, MYSM1 deficiency facilitates the aging process and reduces lifespan, whereas MYSM1 over‐expression attenuates the aging process and increases lifespan in mice. The functional role of MYSM1 is demonstrated in suppressing the aging process and prolonging lifespan. MYSM1 is a key suppressor of aging and may act as a potential agent for the prevention of aging and aging‐associated diseases.