Mitochondria, Inflammation, and Senescence
Cellular senescence is a durable stress-associated state marked by cell-cycle arrest and a pro-inflammatory senescence-associated secretory phenotype (SASP), while mitochondrial dysfunction - defined experimentally by impaired respiratory capacity and membrane potential and commonly accompanied by increased reactive oxygen species (ROS) - both contributes to and results from the senescent phenotype; research has therefore moved from viewing mitochondria primarily as bioenergetic organelles toward examining them as regulators of senescence, inflammatory signaling, stress resistance, and SASP production, and recent work in The FEBS Journal, Journal of Clinical Investigation, Nature, Genes & Development, and Immunity demonstrates sustained interest in mitochondrial dysfunction as a mechanistic bridge connecting cellular stress, chronic inflammation, aging, and age-associated tissue dysfunction.