| Literature DB >> 28729727 |
Bennett G Childs1, Martina Gluscevic1, Darren J Baker1,2, Remi-Martin Laberge3, Dan Marquess3, Jamie Dananberg3, Jan M van Deursen1,2.
Abstract
Chronological age represents the single greatest risk factor for human disease. One plausible explanation for this correlation is that mechanisms that drive ageing might also promote age-related diseases. Cellular senescence, which is a permanent state of cell cycle arrest induced by cellular stress, has recently emerged as a fundamental ageing mechanism that also contributes to diseases of late life, including cancer, atherosclerosis and osteoarthritis. Therapeutic strategies that safely interfere with the detrimental effects of cellular senescence, such as the selective elimination of senescent cells (SNCs) or the disruption of the SNC secretome, are gaining significant attention, with several programmes now nearing human clinical studies.Entities:
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Year: 2017 PMID: 28729727 PMCID: PMC5942225 DOI: 10.1038/nrd.2017.116
Source DB: PubMed Journal: Nat Rev Drug Discov ISSN: 1474-1776 Impact factor: 84.694