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Nuclear and mitochondrial DNA mutate either spontaneously or due to exposure to mutagens. Eukaryotic cells have efficient repair systems to neutralize these mutations. Aging cells (and also young cells in specific genetic variants) lack efficient DNA repair systems, which may lead to activation of oncogenes (like ras), causing oncogene‐induced senescence [30]. Activation of oncogenes in the skin can increase the levels of proteases known as senescence‐associated secretory phenotypes, which can induce early senescence in fibroblasts and keratinocytes [31]. Double‐stranded breaks, mutations, and telomere shortening can affect the overall structure of chromatin in aging cells [32]. Abrogation in the chromatin remodeling mechanism can arrest the cells at G1 checkpoint and can lead to early senescence. A nonfunctional or inhibited histone deacetylase severely affects the chromatin remodeling process and causes early senescence in fibroblasts [33].