BCL2 and myocardial infarction: It also suppresses phosphorylated Jun N-terminal kinase (p-JNK) activation [145], thus leading to the inhibition of mitochondrial apoptotic pathways (B-cell lymphoma-2 (Bcl-2), Bcl-2-associated x-protein (Bax) B-cell lymphoma-extra-large (Bcl-xl), and caspase 3) in the heart of spontaneously hypertensive rats and rodents with myocardial infarction (MI), and in human umbilical vein endothelial cells (HUVECs) subjected to an oxidized low-density lipoprotein-induced model of deep vein thrombosis [127,144,145].