PGC1α is a key regulator of erastin-induced mitochondrial dysfunction during ferroptotic cell death

DOI: 10.5483/bmbrep.2024-0139 Publication Date: 2025-01-22T06:54:02Z
ABSTRACT
A type of programmed cell death called ferroptosis is defined by increased iron-dependent lipid peroxidation. Mitochondria play a central role in iron metabolism. Mitochondrial defects include decreased cristae density, membrane rupture, and mitochondrial which occur as result ferroptosis. One the important regulator biogenesis PGC1α. While recent studies have begun to explore association between PGC1α ferroptosis, specific erastin-induced dysfunction during ferroptotic has not been fully elucidated. In this study, we demonstrate for first time that key mitochondrial-dependent peroxidation HT1080 fibrosarcoma cells. examined function Erastin, an inducer boosted expression Moreover, down-regulation reduced The most biochemical feature increase ion (Fe2+)-dependent peroxide (LOOH) concentration. Mitochondrial-dependent was abolished downregulation. addition, induced potential loss ROS production associated with were blocked inhibition. cells regulated inhibitor. This phenomenon also consistent transfected shRNA Taken together, these results suggest factor death.
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