AI Article Synopsis
- * Mitochondria play a critical role in regulating ferroptosis by producing reactive oxygen species (ROS) and helping maintain cellular stability against oxidative damage.
- * Studies show that the mitochondrial stress response can reduce oxidative stress and ferroptosis in heart muscle cells lacking effective respiration, highlighting its importance in protecting against certain heart diseases linked to mitochondrial dysfunction.
Article Abstract
Ferroptosis is a form of necrotic cell death characterized by iron-dependent lipid peroxidation culminating in membrane rupture. Accumulating evidence links ferroptosis to multiple cardiac diseases and identifies mitochondria as important regulators of ferroptosis. Mitochondria are not only a major source of reactive oxygen species (ROS) but also counteract ferroptosis by preserving cellular redox balance and oxidative defense. Recent evidence has revealed that the mitochondrial integrated stress response limits oxidative stress and ferroptosis in oxidative phosphorylation (OXPHOS)-deficient cardiomyocytes and protects against mitochondrial cardiomyopathy. We summarize the multiple ways in which mitochondria modulate the susceptibility of cells to ferroptosis, and discuss the implications of ferroptosis for cardiomyopathies in mitochondrial disease.
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| http://dx.doi.org/10.1016/j.tcb.2023.06.002 | DOI Listing |
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