ALS-linked SOD1 mutations impair mitochondrial-derived vesicle formation and accelerate aging.

ABSTRACT: Oxidative stress (OS) is regarded as the dominant theory for aging. While compelling correlative data have been generated to support the OS theory, a direct cause-and-effect relationship between the accumulation of oxidation-mediated damage and aging has not been firmly established. Superoxide dismutase 1 (SOD1) is a primary antioxidant in all cells. It is, however, susceptible to oxidation due to OS and gains toxic properties to cells. This study investigates the role of oxidized SOD1 derived from amyotrophic lateral sclerosis (ALS) linked SOD1 mutations in cell senescence and aging. Herein, we have shown that the cell line NSC34 expressing the G93A mutation of human SOD1 (hSOD1^G93A) entered premature senescence as evidenced by a decreased number of the 5-ethynyl-2'-deoxyuridin

SUBMITTER: Guo Y 

PROVIDER: S-EPMC10746562 | biostudies-literature | 2024 Feb

REPOSITORIES: biostudies-literature