A Unifying Mechanism for Mitochondrial Superoxide Production during Ischemia-Reperfusion Injury.

By Edward T. Chouchani, V. Pell, A. James, L. Work, K. Saeb‐Parsy, C. Frezza, T. Krieg, M. Murphy. Cell Metabolism, 2016

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Repurposing mitochondria from ATP production to ROS generation drives a pro-inflammatory phenotype in macrophages that depends on succinate oxidation by complex II (2016, background): “IL-1b Asmitochondrial ROS production is greatly enhanced by both an increase in DJm and an increase in SDH activity (Chouchani et al., 2016), we next examined whether ROS could act as a redox signal emanating frommitochondria to drive IL-1b production.”
Mitochondrial dysfunction: mechanisms and advances in therapy (2024, background): “215 Ca 2 + overload and MPT .”
Mitochondrial ROS promote mitochondrial dysfunction and inflammation in ischemic acute kidney injury by disrupting TFAM-mediated mtDNA maintenance (2021, background): “Mitochondrial ROS (mtROS) are primarily produced at complexes I and III of the electron transport chain (ETC) when electrons derived from either NADH or FADH2 react with O2 [13].”
Ischemia/Reperfusion (2016, neutral): “electron transport at mitochondrial complex I (145, 146).”
Hyperglycemia and Oxidative Stress: An Integral, Updated and Critical Overview of Their Metabolic Interconnections (2023, background): “Thus, aerobic glycolysis could become an important source of superoxide, depending on the integrity of mitochondrial ETC machinery [46].”