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Keywords {🔍}

article, google, scholar, cas, cell, death, necroptosis, myocardial, pgam, necrosis, injury, ischemiareperfusion, wang, liu, inhibition, zhang, nature, peng, ripk, access, regulated, privacy, cookies, content, rat, hearts, protein, luo, jun, pathways, mechanisms, mitochondrial, apoptosis, biol, china, xiangya, university, information, publish, research, search, cardiovascular, phosphoglycerate, mutase, dynaminrelated, xiuju, cells, reperfusion, kinase, drp,

Topics {✒️}

ripk1/ripk3/mlkl-mediated necroptosis contributes rip1/rip3/mlkl-mediated necroptosis month download article/chapter /r-induced myocardial necroptosis myocardial ischemia/reperfusion injury xiu-ju luo pgam5-mediated programmed necrosis nian-sheng li cyclophilin d-overlapping pathways /r-treated heart showed /r-treated rat hearts qi-lin ma yin-zhuang zhang induced myocardial necroptosis induced mitochondrial dysfunctions ischemic/reperfused hearts myocardial ischemia/reperfusion myocardial ischemia-reperfusion mitochondrial pgam5-drp1 signalling article cardiovascular drugs chronic intestinal inflammation dynamin-related protein 1 full article pdf privacy choices/manage cookies multiple necrosis pathways programmed cell death cellular hypoxia/reoxygenation injuries mediating oxidative injury mitochondrial membrane potential ros-dependent apoptosis necrotic cell death related subjects necroptosis-relevant proteins mol cell biol necroptotic cell death cell death differ cell death dis phosphoglycerate mutase 5 sd rat hearts regulated cell death heart fail rev li-jing tang china lang myocardial injury european economic area inhibiting complement activation permeability transition pore calcium-apoptosis link van wijk sjl mouse lung fibroblasts

Questions {❓}

• Regulation of necrotic cell death: p53, PARP1 and cyclophilin D-overlapping pathways of regulated necrosis?

Schema {🗺️}

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         headline:Inhibition of Phosphoglycerate Mutase 5 Reduces Necroptosis in Rat Hearts Following Ischemia/Reperfusion Through Suppression of Dynamin-Related Protein 1
         description:Necroptosis is an important form of cell death following myocardial ischemia/reperfusion (I/R) and phosphoglycerate mutase 5 (PGAM5) functions as the convergent point for multiple necrosis pathways. This study aims to investigate whether inhibition of PGAM5 could reduce I/R-induced myocardial necroptosis and the underlying mechanisms. The SD rat hearts (or H9c2 cells) were subjected to 1-h ischemia (or 10-h hypoxia) plus 3-h reperfusion (or 4-h reoxygenation) to establish the I/R (or H/R) injury model. The myocardial injury was assessed by the methods of biochemistry, H&E (hematoxylin and eosin), and PI/DAPI (propidium iodide/4′,6-diamidino-2-phenylindole) staining, respectively. Drug interventions or gene knockdown was used to verify the role of PGAM5 in I/R (or H/R)-induced myocardial necroptosis and possible mechanisms. The I/R-treated heart showed the injuries (increase in infarct size and creatine kinase release), upregulation of PGAM5, dynamin-related protein 1 (Drp1), p-Drp1-S616, and necroptosis-relevant proteins (RIPK1/RIPK3, receptor-interacting protein kinase 1/3; MLKL, mixed lineage kinase domain-like); these phenomena were attenuated by inhibition of PGAM5 or RIPK1. In H9c2 cells, H/R treatment elevated the levels of PGAM5, RIPK1, RIPK3, MLKL, Drp1, and p-Drp1-S616 and induced mitochondrial dysfunctions (elevation in mitochondrial membrane potential and ROS level) and cellular necrosis (increase in LDH release and the ratio of PI+/DAPI+ cells); these effects were blocked by inhibition or knockdown of PGAM5. Inhibition of PGAM5 can reduce necroptosis in I/R-treated rat hearts through suppression of Drp1; there is a positive feedback between RIPK1 and PGAM5, and PGAM5 might serve as a novel therapeutic target for prevention of myocardial I/R injury.
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      headline:Inhibition of Phosphoglycerate Mutase 5 Reduces Necroptosis in Rat Hearts Following Ischemia/Reperfusion Through Suppression of Dynamin-Related Protein 1
      description:Necroptosis is an important form of cell death following myocardial ischemia/reperfusion (I/R) and phosphoglycerate mutase 5 (PGAM5) functions as the convergent point for multiple necrosis pathways. This study aims to investigate whether inhibition of PGAM5 could reduce I/R-induced myocardial necroptosis and the underlying mechanisms. The SD rat hearts (or H9c2 cells) were subjected to 1-h ischemia (or 10-h hypoxia) plus 3-h reperfusion (or 4-h reoxygenation) to establish the I/R (or H/R) injury model. The myocardial injury was assessed by the methods of biochemistry, H&E (hematoxylin and eosin), and PI/DAPI (propidium iodide/4′,6-diamidino-2-phenylindole) staining, respectively. Drug interventions or gene knockdown was used to verify the role of PGAM5 in I/R (or H/R)-induced myocardial necroptosis and possible mechanisms. The I/R-treated heart showed the injuries (increase in infarct size and creatine kinase release), upregulation of PGAM5, dynamin-related protein 1 (Drp1), p-Drp1-S616, and necroptosis-relevant proteins (RIPK1/RIPK3, receptor-interacting protein kinase 1/3; MLKL, mixed lineage kinase domain-like); these phenomena were attenuated by inhibition of PGAM5 or RIPK1. In H9c2 cells, H/R treatment elevated the levels of PGAM5, RIPK1, RIPK3, MLKL, Drp1, and p-Drp1-S616 and induced mitochondrial dysfunctions (elevation in mitochondrial membrane potential and ROS level) and cellular necrosis (increase in LDH release and the ratio of PI+/DAPI+ cells); these effects were blocked by inhibition or knockdown of PGAM5. Inhibition of PGAM5 can reduce necroptosis in I/R-treated rat hearts through suppression of Drp1; there is a positive feedback between RIPK1 and PGAM5, and PGAM5 might serve as a novel therapeutic target for prevention of myocardial I/R injury.
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