Cardiomyocyte-specific knockout or overexpression of LDHA affects cardiomyocyte proliferation and cardiac repair after MI, mainly due to reduced succinyl coenzyme A inhibition of thioredoxin reductase 1 ubiquitination mediated by LDHA, leading to decreased oxidative stress, promotion of cardiomyocyte proliferation, and even induction of M2 macrophage polarization [135]. Here, LDHA is linked to myocardial infarction.