LAUSR

Aging is considered the contributory accumulation of abruptions occurring through cell signaling cascades, which ultimately cause changes in physical functions, cell fate, and damage across all organ systems. DNA damage response (DDR) also occurs through telomere shortening, tumor formation, mitochondrial dysfunction, and so forth. Cellular aging occurs through cell cycle arrest, which is the result of extended DDR cascade signaling networks via MDC1, 53BP1, H2AX, ATM, ARF, P53, P13‐Akt, BRAF, Sirtuins, NAD + , and so forth. These persistent cell cycle arrests initiated by DDR and other associated stress‐induced signals promote a permanent state of cell cycle arrest called senescence‐associated secretory phenotype (SASP). However, cellular aging gets accelerated with faulty DNA repair systems, and the produced senescent cells further generate various promoting contributors to age‐related dysfunctional diseases including SASP. Any changes to these factors contribute to age‐related disease development. Therefore, this review explores anti‐aging factors targeting DDR and SASP regulation and their detailed signaling networks. In addition, it allows researchers to identify anti‐aging targets and anti‐aging therapeutic strategies based on identified and nonidentified targets.