title: Reactive oxygen species as mediators of cellular senescence.
abstract: Aging has often been viewed as a random process arising from the accumulation of both genetic and epigenetic changes. Increasingly, the notion that aging is a stochastic process is being supplanted by the concept that maximum lifespan of an organism is tightly regulated. This knowledge has led to a growing overlap between classical signal transduction paradigms and the biology of aging. We review certain specific examples where these seemingly disparate disciplines intersect. In particular, we review the concept that intracellular reactive oxygen species function as signalling molecules and that oxidants play a central role as mediators of cellular senescence.
authors.affiliation: Cardiovascular Branch, NHLBI, NIH, Bethesda, Maryland 20892-1454, USA.
authors.forename: Renata
authors.initials: R
authors.lastname: Colavitti
authors.forename: Toren
authors.initials: T
authors.lastname: Finkel
mesh_terms: D000818:Animals; D016922:Cellular Senescence; D005609:Free Radicals; D006801:Humans; D020935:MAP Kinase Signaling System; D008954:Models, Biological; D016877:Oxidants / Q000494:pharmacology; D018384:Oxidative Stress; D010100:Oxygen / Q000378:metabolism; D017382:Reactive Oxygen Species; D015398:Signal Transduction; D019098:Telomerase / Q000378:metabolism; D014158:Transcription, Genetic
chemical_list: D005609:Free Radicals; D016877:Oxidants; D017382:Reactive Oxygen Species; D019098:Telomerase; D010100:Oxygen