We are analyzing https://link.springer.com/article/10.1007/s10565-022-09716-2.

Title:
Mitochondrial quality control in cardiac ischemia/reperfusion injury: new insights into mechanisms and implications | Cell Biology and Toxicology
Description:
The current effective method for the treatment of myocardial infarction is timely restoration of the blood supply to the ischemic area of the heart. Although reperfusion is essential for reestablishing oxygen and nutrient supplies, it often leads to additional myocardial damage, creating an important clinical dilemma. Reports from long-term studies have confirmed that mitochondrial damage is the critical mechanism in cardiac ischemia/reperfusion (I/R) injury. Mitochondria are dynamic and possess a quality control system that targets mitochondrial quantity and quality by modifying mitochondrial fusion, fission, mitophagy, and biogenesis and protein homeostasis to maintain a healthy mitochondrial network. The system of mitochondrial quality control involves complex molecular machinery that is highly interconnected and associated with pathological changes such as oxidative stress, calcium overload, and endoplasmic reticulum (ER) stress. Because of the critical role of the mitochondrial quality control systems, many reports have suggested that defects in this system are among the molecular mechanisms underlying myocardial reperfusion injury. In this review, we briefly summarize the important role of the mitochondrial quality control in cardiomyocyte function and focus on the current understanding of the regulatory mechanisms and molecular pathways involved in mitochondrial quality control in cardiac I/R damage. Graphical abstract
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Keywords {🔍}

pubmed, article, google, scholar, mitochondrial, cas, central, cell, injury, mitophagy, ischemiareperfusion, wang, cardiac, myocardial, zhang, control, quality, biol, heart, fission, protein, mol, res, chen, stress, physiol, liu, zhu, yang, role, protects, httpsdoiorg, zhou, httpsdoiorgs, bnip, apoptosis, reperfusion, biogenesis, death, med, sci, opa, inhibition, autophagy, function, cardiomyocyte, regulates, cardiomyocytes, biochem, mediates,

Topics {✒️}

mitochondrial fission-vdac1-hk2-mptp-mitophagy axis mitophagy-mediated hif-1α/bnip3 pathway month download article/chapter myocardial ischemia/reperfusion-induced apoptosis amp-activated protein kinase hypoxia-inducible pro-apoptotic /r-mediated myocardial injury p-ampk/fundc1 axis lethal ischemia-reperfusion injury attenuate ischemia/reperfusion injury myocardial ischemia-reperfusion injury myocardial ischemia/reperfusion injury cardiac ischemia/reperfusion injury cardiac ischemia-reperfusion injury mitophagy receptor bnip3l/nix akt-creb- pgc1α pathway suppressing fundc1-mediated mitophagy mitochondrial fusion-fission proteins cardiac ischemia-reperfusion injuries mff-required mitochondrial fission fine-tune hypoxic mitophagy myocardial ischaemia/reperfusion injury erk1/2/drp1 signaling pathway oma1-dele1-hri pathway estrogen-related receptor signaling hypoxia-reoxygenation injury bnip3 mediates permeabilization article cell biology phosphorylation-mediated mitochondrial fission subsequent akt/drp1 interaction cardiomyocyte apoptosis induced mitochondrial protein bnip3 improving mitochondrial fusion/mitophagy pink1/parkin-mediated mitophagy integrated stress response er-mitochondrial contact site ck2α-disturbed mitochondrial homeostasis stress response mediated biochim biophys acta full article pdf pink1/parkin-dependent manner mitochondrial quality control hypoxia-reperfusion injury improves cell survival dynamin-related protein 1 dynamin-related protein-1 mitochondrial-nuclear communication ischemia-reperfusion injury ischemia/reperfusion injury mitochondrial fission mediated

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         description:The current effective method for the treatment of myocardial infarction is timely restoration of the blood supply to the ischemic area of the heart. Although reperfusion is essential for reestablishing oxygen and nutrient supplies, it often leads to additional myocardial damage, creating an important clinical dilemma. Reports from long-term studies have confirmed that mitochondrial damage is the critical mechanism in cardiac ischemia/reperfusion (I/R) injury. Mitochondria are dynamic and possess a quality control system that targets mitochondrial quantity and quality by modifying mitochondrial fusion, fission, mitophagy, and biogenesis and protein homeostasis to maintain a healthy mitochondrial network. The system of mitochondrial quality control involves complex molecular machinery that is highly interconnected and associated with pathological changes such as oxidative stress, calcium overload, and endoplasmic reticulum (ER) stress. Because of the critical role of the mitochondrial quality control systems, many reports have suggested that defects in this system are among the molecular mechanisms underlying myocardial reperfusion injury. In this review, we briefly summarize the important role of the mitochondrial quality control in cardiomyocyte function and focus on the current understanding of the regulatory mechanisms and molecular pathways involved in mitochondrial quality control in cardiac I/R damage.
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            Myocardial I/R injury
            Mitophagy
            Mitochondrial biogenesis
            Mitochondrial unfolded protein response
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            Cell Biology
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            Biochemistry
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      description:The current effective method for the treatment of myocardial infarction is timely restoration of the blood supply to the ischemic area of the heart. Although reperfusion is essential for reestablishing oxygen and nutrient supplies, it often leads to additional myocardial damage, creating an important clinical dilemma. Reports from long-term studies have confirmed that mitochondrial damage is the critical mechanism in cardiac ischemia/reperfusion (I/R) injury. Mitochondria are dynamic and possess a quality control system that targets mitochondrial quantity and quality by modifying mitochondrial fusion, fission, mitophagy, and biogenesis and protein homeostasis to maintain a healthy mitochondrial network. The system of mitochondrial quality control involves complex molecular machinery that is highly interconnected and associated with pathological changes such as oxidative stress, calcium overload, and endoplasmic reticulum (ER) stress. Because of the critical role of the mitochondrial quality control systems, many reports have suggested that defects in this system are among the molecular mechanisms underlying myocardial reperfusion injury. In this review, we briefly summarize the important role of the mitochondrial quality control in cardiomyocyte function and focus on the current understanding of the regulatory mechanisms and molecular pathways involved in mitochondrial quality control in cardiac I/R damage.
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         Myocardial I/R injury
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         Mitochondrial biogenesis
         Mitochondrial unfolded protein response
         Mitochondrial dynamics
         Cell Biology
         Pharmacology/Toxicology
         Biochemistry
         general
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