TNNI3 and ischemia: The study found that exogenous ATP and ADP were unable to protect the heart, while mitochondrial transplantation significantly reduced myocardial necrosis and cardiomyocyte apoptosis, markedly decreased infarct size (IS), caspase-3-like activity, TUNEL, as well as the release of creatine kinase isoenzymes (CK-MB) and cardiac troponin I (cTnI), alleviating myocardial injury and significantly enhancing regional and overall myocardial function recovery after ischemia [32].