Abstract
Myocardial reperfusion therapy is the most important therapeutic strategy for myocardial infarction (MI) by reversing myocardial ischemia and reducing the infarct size. However, the ischemia and reperfusion (I/R) injury may dramatically alleviate this therapeutic benefits [ [1] Takemura G. Nakagawa M. Kanamori H. Minatoguchi S. Fujiwara H. Benefits of reperfusion beyond infarct size limitation. Cardiovasc. Res. 2009; 83: 269-276 Crossref PubMed Scopus (43) Google Scholar ]. A series of preclinical studies support the point of view that myocardial I/R injury may involve in a complex pathophysiological process which can further induce cardiac remodeling [ [2] Sun Y. Myocardial repair/remodelling following infarction: roles of local factors. Cardiovasc. Res. 2009; 81: 482-490 Crossref PubMed Scopus (234) Google Scholar ]. Cardiac remodeling leads to progressive heart chamber dilation, ventricular wall thinning, and eventually heart failure [ [3] Murdoch C.E. Zhang M. Cave A.C. Shah A.M. NADPH oxidase-dependent redox signalling in cardiac hypertrophy, remodelling and failure. Cardiovasc. Res. 2006; 71: 208-215 Crossref PubMed Scopus (289) Google Scholar ]. Hence, reversing myocardial I/R injury-induced cardiac remodeling may become a novel therapeutic target.
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