RTN4 and myocardial infarction: Our in vivo functional study in Nogo-C null mice provides solid evidence supporting our hypothesis, that depletion of Nogo-C protected cardiomyocyte apoptosis in MI heart, largely decreased IR, and most importantly, preserved cardiac function after MI injury, suggesting that Nogo-C may serve as a therapeutic target for treatment of MI or ischemia-related cardiac diseases.