Oxidative Stress, Mitochondrial Dysfunction, and Aging

TLDR

Aging is a progressive decline in physiological function linked to increased mortality and disease, and prevailing theories attribute it to cumulative oxidative damage to mitochondria and mtDNA by reactive oxygen species. The paper aims to review the current understanding of how reactive oxygen species and mitochondria interact and to evaluate their potential influence on aging and age‑related diseases. The authors synthesize existing evidence on ROS‑mitochondria interplay, discussing how oxidative damage to mtDNA impairs mitochondrial function, which in turn amplifies ROS production and contributes to aging.

Abstract

Aging is an intricate phenomenon characterized by progressive decline in physiological functions and increase in mortality that is often accompanied by many pathological diseases. Although aging is almost universally conserved among all organisms, the underlying molecular mechanisms of aging remain largely elusive. Many theories of aging have been proposed, including the free-radical and mitochondrial theories of aging. Both theories speculate that cumulative damage to mitochondria and mitochondrial DNA (mtDNA) caused by reactive oxygen species (ROS) is one of the causes of aging. Oxidative damage affects replication and transcription of mtDNA and results in a decline in mitochondrial function which in turn leads to enhanced ROS production and further damage to mtDNA. In this paper, we will present the current understanding of the interplay between ROS and mitochondria and will discuss their potential impact on aging and age-related diseases.