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• W2801266108 endingPage "607" @default.
• W2801266108 startingPage "595" @default.
• W2801266108 abstract "Cellular senescence, in both mitotic and postmitotic cells, can be triggered by various exogenous and endogenous stimuli such as DNA damage, oncogene activation, oxidative stress, telomere dysfunction, and chemotherapeutic drugs. While cellular senescence prevents proliferation of damaged mitotic cells, recent evidence suggests a potential role for postmitotic cell senescence (PoMiCS) in health and disease. Induction of PoMiCS, like cell senescence triggered in mitotic cells, engages numerous tumor suppressors involved in the p53/p21 and p16INK4A/Rb pathways. Similarly to mitotic cells undergoing senescence, cells in PoMiCS secrete a combination of matrix metalloproteases, growth factors, and proinflammatory cytokines, a phenomenon called the senescence-associated secretory phenotype (SASP). Senescent cells promote cellular reprogramming of neighboring cells both in vitro and in vivo and thus, through PoMiCS, could play a critical function in maintaining the integrity of postmitotic tissues in response to stress. In mitotic cells, cellular senescence is a permanent state of G1 arrest, that may have evolved in parallel to apoptosis, to limit proliferation of damaged cells and oncogenesis. Recent studies have suggested that postmitotic cells are also capable of entering a state of senescence, although the repercussions of postmitotic cellular senescence (PoMiCS) on tissue health and function are currently ill-defined. In tissues made largely of post-mitotic cells, it is evolutionary advantageous to preserve cellular integrity and cellular senescence of post-mitotic cells may prevent stressor-induced tissue degeneration and promote tissue repair. Paradoxically, PoMiCS may also contribute to disease progression through the generation of inflammatory mediators, termed the senescence-associated secretory phenotype. Here, we discuss the potential roles of PoMiCS and propose to enlarge the current definition of cellular senescence to postmitotic terminally differentiated cells. In mitotic cells, cellular senescence is a permanent state of G1 arrest, that may have evolved in parallel to apoptosis, to limit proliferation of damaged cells and oncogenesis. Recent studies have suggested that postmitotic cells are also capable of entering a state of senescence, although the repercussions of postmitotic cellular senescence (PoMiCS) on tissue health and function are currently ill-defined. In tissues made largely of post-mitotic cells, it is evolutionary advantageous to preserve cellular integrity and cellular senescence of post-mitotic cells may prevent stressor-induced tissue degeneration and promote tissue repair. Paradoxically, PoMiCS may also contribute to disease progression through the generation of inflammatory mediators, termed the senescence-associated secretory phenotype. Here, we discuss the potential roles of PoMiCS and propose to enlarge the current definition of cellular senescence to postmitotic terminally differentiated cells. a complex cellular response to stress in which the cell remains viable and metabolically active. Cellular senescence is accompanied by important transcriptional changes, reorganization of the chromatin structure, secretion of factors (see SASP and Box 2), and activation of tumor suppressive pathways. In mitotic cells exposed to stressors, induction of cellular senescence is associated with a stable growth arrest. a common complication of both type I and II diabetes, characterized by vascular leakage in the neural retina leading to macular edema, vascular degeneration in the retina, and/or pathological vascular growth on the retinal surface. an intricate network of molecular pathways allowing recognition, signaling, and repair of DNA breaks. cellular senescence triggered following activation of an oncogene, such as Ras, Raf, STAT5, or Cdc6, among others. OIR is a model of retinal vascular diseases, called ischemic retinopathies, characterized by an initial phase of vascular degeneration and followed by a phase of pathological angiogenesis. This model is typically used as a proxy for retinopathy of prematurity and findings can be extrapolated to proliferative diabetic retinopathy. a cell that does not have the ability to divide anymore following its differentiation program. refers to a postmitotic (nondividing) cell that entered senescence in response to stress or during aging. chemically reactive oxygen-derived molecules from endogenous (mitochondria, peroxisomes, etc.) or exogenous (smoke, radiation) sources. central neurons located at the surface of the retina that receive visual information from photoreceptors and interneurons and relay it to the brain. a potentially blinding vascular disease of the retina that affects babies born prematurely. It occurs when the infant spends a significant portion of the 3rd trimester ex-utero and their retinal vasculature does not develop, or degenerates as consequence of oxygen supplementation paradigms. dense chromatin structures occurring in some types of cellular senescence and associated with punctate nuclear DAPI staining as well as enrichment in H3K9me3 and HP1. secretion by senescent cells of a series of matrix metalloproteinases, growth factors, and/or cytokines. a compound promoting the death of senescent cells while sparing quiescent and proliferating cells." @default.
• W2801266108 created "2018-05-17" @default.
• W2801266108 creator A5043973388 @default.
• W2801266108 creator A5086486331 @default.
• W2801266108 date "2018-08-01" @default.
• W2801266108 modified "2023-10-14" @default.
• W2801266108 title "Cellular Senescence in Postmitotic Cells: Beyond Growth Arrest" @default.
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