期刊
TRANSLATIONAL RESEARCH
卷 226, 期 -, 页码 96-104出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.trsl.2020.06.007
关键词
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资金
- National Institutes of Health (NIH) [P01 AG062413, R21 AG065868, K01 AR070241]
- Mayo Clinic Robert and Arlene Kogod Center on Aging
- Richard F. Emslander Career Development Award in Endocrinology
Much of the population is now faced with an enormous burden of age-associated chronic diseases. Recent discoveries in geroscience indicate that healthspan in model organisms such as mice can be manipulated by targeting cellular senescence, a hallmark mechanism of aging, defined as an irreversible proliferative arrest that occurs when cells experience oncogenic or other diverse forms of damage. Senescent cells and their proinflammatory secretome have emerged as contributors to age-related tissue dysfunction and morbidity. Cellular senescence has causal roles in mediating osteoporosis, frailty, cardiovascular diseases, osteoarthritis, pulmonary fibrosis, renal diseases, neurodegenerative diseases, hepatic steatosis, and metabolic dysfunction. Therapeutically targeting senescent cells in mice can prevent, delay, or alleviate each of these conditions. Therefore, senotherapeutic approaches, including senolytics and senomorphics, that either selectively eliminate senescent cells or interfere with their ability to promote tissue dysfunction, are gaining momentum as potential realistic strategies to abrogate human senescence to thereby compress morbidity and extend healthspan.
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