<p>Cellular senescence is the core cytological basis for organismal aging and the development of age-related diseases. Accumulating evidence indicates that senescent phenotypes can be maintained long-term even after the removal of senescence-inducing stressors, and may even affect daughter cells and offspring. This review systematically proposes an integrated theoretical framework of "aging metabolic memory", explaining the persistence, transmissibility, and potential heritability of aging from a systems biology perspective. First, it elaborates on how mitochondrial metabolic reprogramming reshapes the cellular epigenetic landscape (DNA methylation, histone modification) by altering the homeodynamics of key metabolites (NAD⁺, α-ketoglutarate, succinate, etc.), thereby forming stable senescence imprints; second, it in-depth analyzes the mechanisms by which the senescence-associated secretory phenotype (SASP) and extracellular vesicles (EVs) act as "memory carriers" to achieve intercellular transmission and systemic spread of senescent phenotypes; on this basis, combined with the latest progress in epigenetics, it proposes and demonstrates a hypothetical model for the transgenerational transmission of aging metabolic memory through germ cells, exploring its biological significance and evolutionary implications; finally, it systematically sorts out and prospects novel aging intervention strategies based on "memory intervention" (rather than mere elimination), including metabolic resetting, epigenetic remodeling, transmission blocking, and germ cell-targeted intervention. This review summarizes the spatiotemporal dynamic characteristics of aging and may provide multi-dimensional intervention pathways for the precise prevention and treatment of age-related diseases and the promotion of healthy aging.</p>