Progress in Understanding Oxidative Stress, Aging, and Aging-Related Diseases

Abstract

Under normal physiological conditions, reactive oxygen species (ROS) are produced through redox reactions as byproducts of respiratory and metabolic activities. However, due to various endogenous and exogenous factors, the body may produce excessive ROS, which leads to oxidative stress (OS). Numerous studies have shown that OS causes a variety of pathological changes in cells, including mitochondrial dysfunction, DNA damage, telomere shortening, lipid peroxidation, and protein oxidative modification, all of which can trigger apoptosis and senescence. OS also induces a variety of aging-related diseases, such as retinal disease, neurodegenerative disease, osteoarthritis, cardiovascular diseases, cancer, ovarian disease, and prostate disease. In this review, we aim to introduce the multiple internal and external triggers that mediate ROS levels in rodents and humans as well as the relationship between OS, aging, and aging-related diseases. Finally, we present a statistical analysis of effective antioxidant measures currently being developed and applied in the field of aging research.

The Role of Mitochondrial Copy Number in Neurodegenerative Diseases: Present Insights and Future Directions

“…The compromise of ER morphology results in DNA damage, shortening of telomeres, lipid peroxidation and oxidative modification of proteins, triggering cellular oxidative stress and senescence. Cellular senescence promotes the secretion of senescence-associated secretory phenotypes (SASPs), including IL-6, IL-8, and TNF-α, involved in the promotion of chronic inflammation and systemic aging [ 19 ].…”