Functional and clinical repercussions of myocyte apoptosis in the multifaceted damage by ischemia/reperfusion injury: old and new concepts after 10 years of contributions.
Ten years ago, the first finding of apoptotic cell death on the 'crime scene' of cardiac ischemia/reperfusion injury profoundly dismayed the scientific community. This observation jarred with the deeply rooted conviction that cardiac myocytes stoically 'break, but do not bend' in the fight against ischemia, instead of spontaneously accepting a peaceful demise for the greater good. Ten years later, a number of studies not only proved right the coexistence of necrosis and apoptosis on the ischemic battle field, but also implicated myocyte apoptosis in the pathogenesis of all the shapes and shades that cardiac ischemic injury can take on.
Scarabelli
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Center for Heart and Vessel Preclinical Studies, Division of Cardiology, St. John Hospital, Wayne State University, 22201 Moross Road, Detroit, MI 48336, USA. tiziano.scarabelli@stjohn.org
Gottlieb
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D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D016923:Cell Death / Q000502:physiology; D006801:Humans; D008929:Mitochondria, Heart / Q000502:physiology; D017202:Myocardial Ischemia / Q000473:pathology* / Q000503:physiopathology; D015428:Myocardial Reperfusion Injury / Q000473:pathology* / Q000503:physiopathology; D032383:Myocytes, Cardiac / Q000473:pathology*