The role of RIPK3‐regulated cell death pathways and necroptosis in the pathogenesis of cardiac ischaemia‐reperfusion injury

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Inhibition of Phosphoglycerate Mutase 5 Reduces Necroptosis in Rat Hearts Following Ischemia/Reperfusion Through Suppression of Dynamin-Related Protein 1

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ZYZ-803 Mitigates Endoplasmic Reticulum Stress-Related Necroptosis after Acute Myocardial Infarction through Downregulating the RIP3-CaMKII Signaling Pathway

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Promoting effect of baicalin on nitric oxide production in CMECs via activating the PI3K-AKT-eNOS pathway attenuates myocardial ischemia–reperfusion injury

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Neutrophil-derived advanced glycation end products-Nε-(carboxymethyl) lysine promotes RIP3-mediated myocardial necroptosis via RAGE and exacerbates myocardial ischemia/reperfusion injury

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Inhibitory effect of melatonin on necroptosis via repressing the Ripk3-PGAM5-CypD-mPTP pathway attenuates cardiac microvascular ischemia-reperfusion injury

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Ripk3 promotes ER stress-induced necroptosis in cardiac IR injury: A mechanism involving calcium overload/XO/ROS/mPTP pathway

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Targeting necroptotic cell death pathway by high-intensity interval training (HIIT) decreases development of post-ischemic adverse remodelling after myocardial ischemia / reperfusion injury

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Melatonin attenuates chronic pain related myocardial ischemic susceptibility through inhibiting RIP3-MLKL/CaMKII dependent necroptosis

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Sorafenib tosylate inhibits directly necrosome complex formation and protects in mouse models of inflammation and tissue injury

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Ripk3 induces mitochondrial apoptosis via inhibition of FUNDC1 mitophagy in cardiac IR injury

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Inhibition of mitochondrial fission as a molecular target for cardioprotection: critical importance of the timing of treatment

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PGAM5-mediated programmed necrosis of hepatocytes drives acute liver injury

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Heat shock protein 70 inhibits cardiomyocyte necroptosis through repressing autophagy in myocardial ischemia/reperfusion injury

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MicroRNA-223-5p and -3p Cooperatively Suppress Necroptosis in Ischemic/Reperfused Hearts

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CaMKII is a RIP3 substrate mediating ischemia- and oxidative stress–induced myocardial necroptosis

(2016) Ting Zhang et al.   NATURE MEDICINE

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Necroptosis and its role in inflammation

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A cellular screen identifies ponatinib and pazopanib as inhibitors of necroptosis

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RIPK3-Mediated Necroptosis Regulates Cardiac Allograft Rejection

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RIP3, a kinase promoting necroptotic cell death, mediates adverse remodelling after myocardial infarction

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RIPK1 Blocks Early Postnatal Lethality Mediated by Caspase-8 and RIPK3

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Distinct roles of RIP1–RIP3 hetero- and RIP3–RIP3 homo-interaction in mediating necroptosis

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RIP3 Induces Apoptosis Independent of Pronecrotic Kinase Activity

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RIPK1 maintains epithelial homeostasis by inhibiting apoptosis and necroptosis

(2014) Marius Dannappel et al.   NATURE

Activity of Protein Kinase RIPK3 Determines Whether Cells Die by Necroptosis or Apoptosis

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Depletion of RIPK3 or MLKL blocks TNF-driven necroptosis and switches towards a delayed RIPK1 kinase-dependent apoptosis

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MLKL Compromises Plasma Membrane Integrity by Binding to Phosphatidylinositol Phosphates

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Mechanisms of CaMKII Activation in the Heart

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Study of Cardioprotective Effects of Necroptosis Inhibitors on Isolated Rat Heart Subjected to Global Ischemia–Reperfusion

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Programmed necrosis, not apoptosis, is a key mediator of cell loss and DAMP-mediated inflammation in dsRNA-induced retinal degeneration

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Combination of necroptosis and apoptosis inhibition enhances cardioprotection against myocardial ischemia–reperfusion injury

(2013) Shizuka Koshinuma et al.   Journal of Anesthesia

Myocardial ischemia-reperfusion injury: a neglected therapeutic target

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Mitigation of postischemic cardiac contractile dysfunction by CaMKII inhibition: effects on programmed necrotic and apoptotic cell death

(2013) Adrian Szobi et al.   MOLECULAR AND CELLULAR BIOCHEMISTRY

Plasma membrane translocation of trimerized MLKL protein is required for TNF-induced necroptosis

(2013) Zhenyu Cai et al.   NATURE CELL BIOLOGY

Interferon-induced RIP1/RIP3-mediated necrosis requires PKR and is licensed by FADD and caspases

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Mechanisms of Cell Death in Heart Disease

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Inhibition of RIP1-dependent necrosis prevents adverse cardiac remodeling after myocardial ischemia–reperfusion in vivo

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Necrostatin-1 analogues: critical issues on the specificity, activity and in vivo use in experimental disease models

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The Adaptor Protein FADD Protects Epidermal Keratinocytes from Necroptosis In Vivo and Prevents Skin Inflammation

(2011) Marion C. Bonnet et al.   IMMUNITY

FADD prevents RIP3-mediated epithelial cell necrosis and chronic intestinal inflammation

(2011) Patrick-Simon Welz et al.   NATURE

Catalytic activity of the caspase-8–FLIPL complex inhibits RIPK3-dependent necrosis

(2011) Andrew Oberst et al.   NATURE

Caspase 8 inhibits programmed necrosis by processing CYLD

(2011) Marie Anne O’Donnell et al.   NATURE CELL BIOLOGY

Toll-like receptors activate programmed necrosis in macrophages through a receptor-interacting kinase-3-mediated pathway

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Phosphorylation-Driven Assembly of the RIP1-RIP3 Complex Regulates Programmed Necrosis and Virus-Induced Inflammation

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Adjunctive Thrombectomy and Distal Protection in Primary Percutaneous Coronary Intervention

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Identification of RIP1 kinase as a specific cellular target of necrostatins

(2008) Alexei Degterev et al.   Nature Chemical Biology