Transient senescence, whereby damaged cells are eliminated, clearly has beneficial effects for an organism. Furthermore, recent evidence has emerged that senescence also plays a key role in the healing of wounds, tissue repair and during embryonic development. Most notably, it has been suggested that senescence has evolved as a cellular process to avert cell replication on a damaged DNA template, therefore acting as an effective mechanism to prevent tumour progression. It has been demonstrated that senescence can occur as a consequence of oxidative stress, oncogene activation or chromatin modifications, amongst other forms of stress. It is now well established that senescence is a biological programme that can occur in response to a number of stresses and is a feature in multiple physiological and pathological processes. It has since been established that this initial observation reflects a specific type of senescence that occurs in response to telomere attrition. SASP, senescence associated secretory phenotypeĬellular senescence was first described in cultured normal human fibroblasts when it was observed that they ceased to proliferate following a finite number of cell divisions. NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells NAMPT, nicotinamide phosphoribosyltransferase MOTS-c, mitochondrial open reading frame of the 12S rRNA-c MitoTAM, mitochondrial targeted tamoxifen MiMOMP, minority mitochondrial outer membrane permeabilisation MiDAS, mitochondrial dysfunction-associated senescence
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