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Cellular senescence in age-related disorders.

Authors
  • Kaur, Japneet1
  • Farr, Joshua N2
  • 1 Division of Endocrinology, Mayo Clinic College of Medicine, Mayo Clinic, Rochester Minnesota; Robert and Arlene Kogod Center on Aging, Mayo Clinic College of Medicine, Mayo Clinic, Rochester Minnesota.
  • 2 Division of Endocrinology, Mayo Clinic College of Medicine, Mayo Clinic, Rochester Minnesota; Robert and Arlene Kogod Center on Aging, Mayo Clinic College of Medicine, Mayo Clinic, Rochester Minnesota; Division of Physiology and Biomedical Engineering; Mayo Clinic College of Medicine, Mayo Clinic, Rochester, Minnesota. Electronic address: [email protected]
Type
Published Article
Journal
Translational research : the journal of laboratory and clinical medicine
Publication Date
Dec 01, 2020
Volume
226
Pages
96–104
Identifiers
DOI: 10.1016/j.trsl.2020.06.007
PMID: 32569840
Source
Medline
Language
English
License
Unknown

Abstract

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. Copyright © 2020 Elsevier Inc. All rights reserved.

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