Fig. 1.

Dysregulated inflammation, alteration of epigenetic modifications, and metabolic imbalance converge to cell senescence and ageing. Cross talks among epigenetic modifiers (writers, readers, and erasers), inflammatory gene expression and immune cell response, and metabolic alterations contribute to senescent phenotypes and organ degeneration. MiDAS mitochondrial dysfunction-associated senescence, SASP senescence-associated secretory phenotype, OXPHOS oxidative phosphorylation, ROS reactive oxygen species, TCA tricarboxylic acid