TIGAR coordinates senescence-associated secretory phenotype via lysosome repositioning and α-tubulin deacetylation.

ABSTRACT: TP53-induced glycolysis and apoptosis regulator (TIGAR) regulates redox homeostasis and provides the intermediates necessary for cell growth by reducing the glycolytic rate. During cellular senescence, cells undergo metabolic rewiring towards the glycolytic pathway, along with the development of the senescence-associated secretory phenotype (SASP), also known as the secretome. We observed that TIGAR expression increased during replicative senescence following the in vitro expansion of human mesenchymal stromal cells (MSCs) and that TIGAR knockout (KO) decreased SASP factors and triggered premature senescence with decelerated progression. Additionally, TIGAR KO impaired flexible lysosomal movement to the perinuclear region and decreased the autophagic flux of MSCs. Research on the mechanism

SUBMITTER: Nam HY 

PROVIDER: S-EPMC11671532 | biostudies-literature | 2024 Dec

REPOSITORIES: biostudies-literature