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- W1891001446 abstract "Acute myocardial ischemia is the leading cause of morbidity and mortality worldwide [ 1 Zhou X. Sheng X. Chen M. Wang Z. Yu L. Jiang H. Tumor necrosis factor-α inhibitor: a promising therapeutic approach for attenuating myocardial ischemia–reperfusion by antioxidant stress. Int. J. Cardiol. 2015; 190: 282-283 Abstract Full Text Full Text PDF PubMed Scopus (3) Google Scholar , 2 Lee S.M. Hutchinson M. Staikopoulos V. Saint D.A. Amitriptyline pharmacologically preconditions rat hearts against cardiac ischemic–reperfusion injury. Int. J. Cardiol. 2015; 190: 353-359 Abstract Full Text Full Text PDF PubMed Scopus (9) Google Scholar ]. Although abrupt restoration of coronary blood flow would rescue ischemic myocardium, reduce infarct size, attenuate cardiac remodeling and improve systolic function, the additional cardiomyocyte damage and myocardial fibrosis usually could not be evitable [ [3] Chen M. Yu L. Liu Q. Jiang H. Zhou S. Interleukin-17 inhibition: an important target for attenuating myocardial ischemia and reperfusion injury. Int. J. Cardiol. 2015; 198: 89-90 Abstract Full Text Full Text PDF PubMed Scopus (6) Google Scholar ]. This damage is defined as myocardial ischemic reperfusion injury (MIRI). Currently, there is still a lack of effective strategies for attenuating MIRI. Therefore, alternative favorable treatment is urgently needed to reduce cardiomyocyte loss and minimize myocardial fibrosis." @default.
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- W1891001446 date "2015-11-01" @default.
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- W1891001446 title "MG53 protein: A promising novel therapeutic target for myocardial ischemia reperfusion injury" @default.
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- W1891001446 doi "https://doi.org/10.1016/j.ijcard.2015.07.084" @default.
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