On the other hand, there is evidence that leptin was able to inhibit apoptosis of cardiac myocytes and reduce severity of myocardial dysfunction in acute myocardial infarction model and ensured antiproliferative effects through stimulation of cardiac STAT3, PI3K, and Akt activity and mitochondrial function, and also leptin stimulated vascular reparation via nitric oxide–p38 MAP kinase–dependent mechanism (106–108). Here, LEP is linked to acute myocardial infarction.