Abstract Aging is a progressive, systemic decline in biological function driven by interconnected molecular and cellular processes that accumulate across the lifespan. Contemporary mechanistic models conceptualize aging as an emergent phenomenon arising from genomic instability, telomere attrition, epigenetic remodeling, proteostatic collapse, metabolic dysregulation, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. These processes are evolutionarily conserved and experimentally modifiable. This chapter synthesizes mechanistic evidence across model organisms and mammalian systems and evaluates translational strategies aimed at extending healthspan.