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Cellular senescence
Phenomenon characterized by the cessation of cell division / From Wikipedia, the free encyclopedia
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Cellular senescence is a phenomenon characterized by the cessation of cell division.[1][2][3] In their experiments during the early 1960s, Leonard Hayflick and Paul Moorhead found that normal human fetal fibroblasts in culture reach a maximum of approximately 50 cell population doublings before becoming senescent.[4][5][6] This process is known as "replicative senescence", or the Hayflick limit. Hayflick's discovery of mortal cells paved the path for the discovery and understanding of cellular aging molecular pathways.[7] Cellular senescence can be initiated by a wide variety of stress inducing factors. These stress factors include both environmental and internal damaging events, abnormal cellular growth, oxidative stress, autophagy factors, among many other things.[8]
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Bottom: MEFs became senescent after passages. Cells grow larger, flatten shape and expressed senescence-associated β-galactosidase (SABG, blue areas), a marker of cellular senescence.
The physiological importance for cell senescence has been attributed to prevention of carcinogenesis, and more recently, aging, development, and tissue repair.[9] Senescent cells contribute to the aging phenotype, including frailty syndrome, sarcopenia, and aging-associated diseases.[10] Senescent astrocytes and microglia contribute to neurodegeneration.[11][12]