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Rip1 (Receptor-interacting protein kinase 1) mediates necroptosis and contributes to renal ischemia/reperfusion injury
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Rip1 (Receptor-interacting protein kinase 1) mediates necroptosis and contributes to renal ischemia/reperfusion injury
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Journal Article
Rip1 (Receptor-interacting protein kinase 1) mediates necroptosis and contributes to renal ischemia/reperfusion injury
2012
Overview
Loss of kidney function in renal ischemia/reperfusion injury is due to programmed cell death, but the contribution of necroptosis, a newly discovered form of programmed necrosis, has not been evaluated. Here, we identified the presence of death receptor–mediated but caspase-independent cell death in murine tubular cells and characterized it as necroptosis by the addition of necrostatin-1, a highly specific receptor-interacting protein kinase 1 inhibitor. The detection of receptor-interacting protein kinase 1 and 3 in whole-kidney lysates and freshly isolated murine proximal tubules led us to investigate the contribution of necroptosis in a mouse model of renal ischemia/reperfusion injury. Treatment with necrostatin-1 reduced organ damage and renal failure, even when administered after reperfusion, resulting in a significant survival benefit in a model of lethal renal ischemia/reperfusion injury. Unexpectedly, specific blockade of apoptosis by zVAD, a pan-caspase inhibitor, did not prevent the organ damage or the increase in urea and creatinine in vivo in renal ischemia/reperfusion injury. Thus, necroptosis is present and has functional relevance in the pathophysiological course of ischemic kidney injury and shows the predominance of necroptosis over apoptosis in this setting. Necrostatin-1 may have therapeutic potential to prevent and treat renal ischemia/reperfusion injury.
Publisher
Elsevier Inc,Nature Publishing Group,Elsevier Limited
Subject
/ Biological and medical sciences
/ Cysteine Proteinase Inhibitors - pharmacology
/ Humans
/ ischemia
/ Kidney Tubules, Proximal - drug effects
/ Kidney Tubules, Proximal - enzymology
/ Kidney Tubules, Proximal - pathology
/ Male
/ Mice
/ Necrosis
/ Nephrology. Urinary tract diseases
/ Nephropathies. Renovascular diseases. Renal failure
/ Oligopeptides - pharmacology
/ Protein Kinase Inhibitors - pharmacology
/ Receptor-Interacting Protein Serine-Threonine Kinases - antagonists & inhibitors
/ Receptor-Interacting Protein Serine-Threonine Kinases - physiology
/ Reperfusion Injury - enzymology
/ Reperfusion Injury - etiology
