Caveolin-3: a molecular insight into diseases of the heart

Caveolin-3 is protein on the membrane of cardiac myocytes correlated with a variety of cardiovascular diseases. The functional significance of the Cav-3 has been proved by the fact that Cav-3 overexpression or knockdown results in the occurrence and development of cardiovascular disease. Mutations in the gene encoding Cav-3 cause a broad spectrum of clinical phenotypes, ranging from isolated hyperCKemia to most cardiomyopathy and the effect of cav-3 mutations on current density parallels the effect on channel trafficking. Mutations in the Cav-3 gene, such as F97C and S141R, promote ventricular arrhythmogenesis in LQT9 by combined decrease in loss of IK1 and gain of Ina-L. Major changes in the T-tubule system by Cav-3 mutation, which contribute to the regulation of Ca2+ channels, result Cardiac hypertrophy. Furthermore, Cav-3 knockdown (KO) could induce apoptosis initiated by myocardial ischemia/reperfusion injury and many materials, such as volatile anesthetic gas, facilitate cardioprotection by involving AMP-activated protein kinase (AMPK) and cav-3 dependent cyclooxygenase-2 inhibition. This review highlights the overviews that the roles of Cav-3 play in cardiovascular disease, particularly on the arrhythmias and cardiomyopathy.