Mitochondrial and mitochondrial-independent pathways of myocardial cell death during ischaemia and reperfusion injury
Davidson, Sean M. (University College London)
Adameová, Adriana (Comenius University Bratislava)
Barile, Lucio (Università Svizzera Italiana)
Cabrera-Fuentes, H. A. (Justus-Liebig-University)
Lazou, A. (Aristotle University of Thessaloniki)
Pagliaro, Pasquale (University of Turin)
Stensløkken, Kåre-Olav (University of Oslo)
García-Dorado, David (Hospital Universitari Vall d'Hebron. Institut de Recerca)
Universitat Autònoma de Barcelona

Data:	2020
Resum:	Acute myocardial infarction causes lethal injury to cardiomyocytes during both ischaemia and reperfusion (IR). It is important to define the precise mechanisms by which they die in order to develop strategies to protect the heart from IR injury. Necrosis is known to play a major role in myocardial IR injury. There is also evidence for significant myocardial death by other pathways such as apoptosis, although this has been challenged. Mitochondria play a central role in both of these pathways of cell death, as either a causal mechanism is the case of mitochondrial permeability transition leading to necrosis, or as part of the signalling pathway in mitochondrial cytochrome c release and apoptosis. Autophagy may impact this process by removing dysfunctional proteins or even entire mitochondria through a process called mitophagy. More recently, roles for other programmed mechanisms of cell death such as necroptosis and pyroptosis have been described, and inhibitors of these pathways have been shown to be cardioprotective. In this review, we discuss both mitochondrial and mitochondrial-independent pathways of the major modes of cell death, their role in IR injury and their potential to be targeted as part of a cardioprotective strategy. This article is part of a special Issue entitled 'Mitochondria as targets of acute cardioprotection' and emerged as part of the discussions of the European Union (EU)-CARDIOPROTECTION Cooperation in Science and Technology (COST) Action, CA16225.
Drets:	Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original.
Llengua:	Anglès
Document:	Article de revisió ; Article ; Versió publicada
Matèria:	Apoptosis ; Autophagy ; Cardiac ; Cell death ; Ischaemia ; Myocardial infarction ; Necroptosis ; Necrosis ; Pyroptosis ; Reperfusion
Publicat a:	Journal of Cellular and Molecular Medicine, Vol. 24 (march 2020) , p. 3795-3806, ISSN 1582-4934

DOI: 10.1111/jcmm.15127
PMID: 32155321

12 p, 516.3 KB

El registre apareix a les col·leccions:
Articles > Articles publicats