MIF and myocardial infarction: Besides, the plasmid transduction of macrophage migration inhibitory factor (MIF) in bone marrow-MSCs (BM-MSCs) can generate optimized exosomes to result in decreased mitochondrial injury, reactive oxygen species generation, and cell apoptosis of cardiomyocyte under the situation of hypoxia/serum deprivation which greatly restored heart function and reduced heart remodeling in a rat model of MI [111].