Abstract
<jats:p>Reactive oxygen species (ROS) are created by redox reactions as byproducts of respiratory and metabolic processes under normal physiological settings. However, the body may produce excessive ROS due to a variety of endogenous and external sources, which results in oxidative stress. Numerous investigations have demonstrated that oxidative stress induces a range of pathological alterations in cells, including telomere shortening, DNA damage, mitochondrial dysfunction, lipid peroxidation, and protein oxidative modification, all of which can result in senescence and apoptosis. Senescent cell accumulation can, in fact, restrict appropriate tissue renewal and impair organ function. In order to promote healthy aging and reduce age-related illnesses, various theories have been suggested, and research has been performed. We have tried to consolidate the recent approaches involving omics and system biology, caloric restriction, and therapeutic interventions. The dual nature of ROS was deciphered in cellular signaling and maintaining aging-related processes.</jats:p>