Necrostatin‐1 alleviates reperfusion injury following acute myocardial infarction in pigs

In rodents, it has previously been shown that necrostatin‐1 (Nec‐1) inhibits RIP1, a central regulator of programmed necrosis, thereby decreasing cell death and reducing infarct size (IS) after ischaemia/reperfusion (I/R) injury. To address unanswered questions on feasibility and efficacy of Nec‐1 in a large animal model, we assessed the effects of Nec‐1 in a porcine I/R model, relevant to human disease.

[1]  S. Cullen,et al.  RIPK1 can function as an inhibitor rather than an initiator of RIPK3‐dependent necroptosis , 2014, The FEBS journal.

[2]  Seamus J. Martin,et al.  Inflammatory outcomes of apoptosis, necrosis and necroptosis , 2014, Biological chemistry.

[3]  Florian Reisinger,et al.  RIP3, a kinase promoting necroptotic cell death, mediates adverse remodelling after myocardial infarction. , 2014, Cardiovascular research.

[4]  Talicia A Tarver HEART DISEASE AND STROKE STATISTICS–2014 UPDATE: A REPORT FROM THE AMERICAN HEART ASSOCIATION , 2014 .

[5]  D. Green,et al.  Widespread mitochondrial depletion via mitophagy does not compromise necroptosis. , 2013, Cell reports.

[6]  D. Green,et al.  Two independent pathways of regulated necrosis mediate ischemia–reperfusion injury , 2013, Proceedings of the National Academy of Sciences.

[7]  P. Doevendans,et al.  Targeting cell death in the reperfused heart: pharmacological approaches for cardioprotection. , 2013, International journal of cardiology.

[8]  L. V. Van Laake,et al.  Translating cardioprotection for patient benefit: position paper from the Working Group of Cellular Biology of the Heart of the European Society of Cardiology. , 2013, Cardiovascular research.

[9]  G. Heusch Cardioprotection: chances and challenges of its translation to the clinic , 2013, The Lancet.

[10]  P. Doevendans,et al.  Transendocardial cell injection is not superior to intracoronary infusion in a porcine model of ischaemic cardiomyopathy: a study on delivery efficiency , 2012, Journal of cellular and molecular medicine.

[11]  P. Doevendans,et al.  Inhibition of RIP1-dependent necrosis prevents adverse cardiac remodeling after myocardial ischemia–reperfusion in vivo , 2012, Basic Research in Cardiology.

[12]  G. Pasterkamp,et al.  Treatment With OPN-305, a Humanized Anti–Toll-Like Receptor-2 Antibody, Reduces Myocardial Ischemia/Reperfusion Injury in Pigs , 2012, Circulation. Cardiovascular interventions.

[13]  G. Kung,et al.  Programmed necrosis, not apoptosis, in the heart. , 2011, Circulation research.

[14]  H. Bøtker,et al.  Translating novel strategies for cardioprotection: the Hatter Workshop Recommendations , 2010, Basic Research in Cardiology.

[15]  P. Ferdinandy,et al.  Postconditioning and protection from reperfusion injury: where do we stand? Position paper from the Working Group of Cellular Biology of the Heart of the European Society of Cardiology. , 2010, Cardiovascular research.

[16]  M. Ruiz-Meana,et al.  Lethal reperfusion injury in acute myocardial infarction: facts and unresolved issues. , 2009, Cardiovascular research.

[17]  G. Heusch,et al.  Loss of cardioprotection with ageing. , 2009, Cardiovascular research.

[18]  D. Yellon,et al.  The mitochondrial permeability transition pore as a target for preconditioning and postconditioning , 2009, Basic Research in Cardiology.

[19]  P. Doevendans,et al.  Exenatide reduces infarct size and improves cardiac function in a porcine model of ischemia and reperfusion injury. , 2009, Journal of the American College of Cardiology.

[20]  M. Mocanu,et al.  The Cardioprotective Effect of Necrostatin Requires the Cyclophilin-D Component of the Mitochondrial Permeability Transition Pore , 2007, Cardiovascular Drugs and Therapy.

[21]  D. Yellon,et al.  Necrostatin: A Potentially Novel Cardioprotective Agent? , 2007, Cardiovascular Drugs and Therapy.

[22]  Richard B Devereux,et al.  Recommendations for chamber quantification: a report from the American Society of Echocardiography's Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardio , 2005, Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography.

[23]  Alexei Degterev,et al.  Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury , 2005, Nature chemical biology.

[24]  M. Daemen,et al.  The infarcted myocardium: simply dead tissue, or a lively target for therapeutic interventions. , 1999, Cardiovascular research.

[25]  F. Crea,et al.  Contemporary Reviews in Cardiovascular Medicine Mechanisms of Coronary Artery Spasm , 2011 .

[26]  L. Becker Myocardial Reperfusion Injury , 2004, Journal of Thrombosis and Thrombolysis.