Document Detail

Pathophysiology of Myocardial Reperfusion Injury: Preconditioning, Postconditioning and Translational Aspects of Protective Measures.
MedLine Citation:
PMID:  21856909     Owner:  NLM     Status:  Publisher    
Heart diseases due to myocardial ischemia, such as myocardial infarction or ischemic heart failure, are major causes of death in developed countries, and their number is unfortunately still growing. Preliminary exploration into the pathophysiology of ischemia-reperfusion injury, together with the accumulation of clinical evidence, led to the discovery of ischemic preconditioning, which has been the main hypothesis for over three decades for how ischemia-reperfusion injury can be attenuated. The subcellular pathophysiological mechanism of ischemia/reperfusion injury and preconditioning-induced cardioprotection is not well understood; but extensive research into components, including autacoids, ion channels, receptors, subcellular signaling cascades and mitochondrial modulators, as well as strategies for modulating these components, have made evolutional progress. Owing to the accumulation of both basic and clinical evidence, the idea of ischemic postconditioning with a cardioprotective potential has been discovered and established, making it possible to apply this knowledge in the clinical setting after ischemia/reperfusion insult. Another great outcome has been the launch of translational studies that apply basic findings for manipulating ischemia/reperfusion injury into practical clinical treatments against ischemic heart diseases. In this review, we discuss the current findings regarding the fundamental pathophysiological mechanisms of ischemia-reperfusion injury, the associated protective mechanisms of ischemic pre/postconditioning, and the potential seeds for molecular, pharmacological or mechanical treatments against ischemia/reperfusion injury as well as subsequent adverse outcomes by modulation of subcellular signaling mechanisms (especially mitochondrial function). We also review emerging translational clinical trials and the subsistent clinical co-morbidities that need to be overcome to make these trials applicable in clinical medicine.
Shoji Sanada; Issei Komuro; Masafumi Kitakaze
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-8-19
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  -     ISSN:  1522-1539     ISO Abbreviation:  -     Publication Date:  2011 Aug 
Date Detail:
Created Date:  2011-8-22     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
1Osana University Graduate School of Medicine.
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