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Oxid Med Cell Longev 2014:360438 Conrad M, Pratt DA (2019) The chemical basis of ferroptosis

Mitochondrial Dysfunction and Oxidative Stress Oxaliplatin causes morphological changes and functional deficits of mitochondria

Only at high concentrations does DHODH inhibitor exhibit significant sensitization towards ferroptosis, while also effectively suppressing FSP1 activity [137]

Additionally, the variability in individual responses to alcohol presents a challenge in understanding the relationship between ethanol consumption and depression

Crosstalk with mitochondria occurs at ERmitochondria contact sites (MAMs), where tightly coupled Ca and lipid exchange can propagate ROS signals bidirectionallyER stress can potentiate mitochondrial ROS production and mitochondrial dysfunction can feed back to intensify ER oxidative pressureshaping cell-wide redox tone and stress adaptation

doi: 10.1111/j.1532-950x.1993.tb00426.x 92 HuangB.KrafftP