Targeting cell death.
Functional consequences of myocardial or cerebral infarction are the result of excessive cell death. It is patent that preventing cell death is the therapeutic goal in any ischemia-reperfusion setting. Mitochondria amplify apoptotic cascades and have emerged as crucial organelles in ischemia-reperfusion. Changes in mitochondrial inner membrane permeability and in the morphology of the organelle are regulated, perhaps interconnected processes that are starting to emerge as novel therapeutic targets for reducing cell death induced by ischemia-reperfusion.
Hausenloy
D J
DJ
The Hatter Cardiovascular Institute, University College London Hospital, London, UK.
Scorrano
L
L
D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D002317:Cardiovascular Agents / Q000494:pharmacology* / Q000627:therapeutic use; D006801:Humans; D008929:Mitochondria, Heart / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D033681:Mitochondrial Membrane Transport Proteins / Q000037:antagonists & inhibitors* / Q000378:metabolism; D051336:Mitochondrial Membranes / Q000187:drug effects / Q000378:metabolism; D000083162:Mitochondrial Permeability Transition Pore; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D010539:Permeability
D002317:Cardiovascular Agents; D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore