Senescence in Post-Mitotic Cells: A Driver of Aging?

Significance: Cell senescence was originally defined by an acute loss of replicative capacity and thus believed to be restricted proliferation-competent cells. More recently, has been recognized as a cellular stress damage response encompassing multiple pathways or domains, namely DNA response, cell cycle arrest, senescence-associated secretory phenotype, mitochondrial dysfunction, autophagy/mitophagy nutrient signaling, epigenetic reprogramming. Each these domains is activated during senescence, all appear interact with each other. identified important driver mammalian aging. Recent Advances: Activation now also observed in wide range post-mitotic cells, suggesting that can occur nondividing cells temporally uncoupled from arrest. Here, we review recent evidence for speculate about its possible relevance Critical Issues: Although majority found aging, independent confirmation results still lacking most them. Future Directions: To define whether plays significant role aging phenotypes tissues such brain, muscle, heart, others. Antioxid. Redox Signal. 34, 308–323.