Figure 6.

MQS in cardiomyocyte fate regulation (apoptosis, necrosis, necroptosis, pyroptosis, autophagic cell death). MQS fully participates in apoptotic or necrotic cardiomyocyte death. Under ischemic/hypoxic stress, intracellular ROS are overproduced and accompanied by intracellular Ca²⁺ overload. Ischemic stress also breaks the balance between Drp1/FIS1/Mff-mediated mitochondrial fission and OPA1/Mfn1/Mfn2-mediated mitochondrial fusion, which leads to mitochondrial fragmentation and structurally abnormal mitochondria. Mitochondrial autophagy mediated by FUNDC1/Parkin /BNIP3 and NIX is enhanced, leading to PGC1α- and Nrf1/2-mediated decreases in mitochondrial biosynthesis, abnormal opening of mPTPs, and excessive release of Cyto-c into the cytosol. Dysregulation of the mitochondrial electron transport chain and tricarboxylic acid cycle leads to insufficient ATP production. Expression levels of RIPK3 and MLKL are increased, as is activation of caspase-3/-12 and levels of cardiomyocyte.