Author(s)

Jiang Hui

Corresponding Author

Jiang Hui

Abstract

Myocardial hypertrophy is an adaptive response of myocardium to various stimuli, but long-term myocardial hypertrophy is recognized as an independent risk factor for multiple cardiovascular complications. Calmodulin kinase II (CaMK II) activity and expression were significantly increased in hypertrophic myocardium induced by alcohol. Ca2+/CaM-dependent CaMK II signal transduction pathway plays a key role in the formation of hypertrophy and the occurrence of ventricular arrhythmia in hypertrophic myocardium. Abnormal phosphorylation of nuclear transcription factor CREB also plays an important role in transcriptional regulation of myocardial hypertrophy gene. However, it is unclear whether CaMII mediates alcohol-induced cardiac hypertrophy through CREB phosphorylation. Persistent cardiac hypertrophy due to long-term stress can eventually lead to dilated cardiomyopathy, heart failure, and sudden death. The CaMKII signal transduction pathway is expected to be a new target for clinical cardiac hypertrophy and arrhythmia prevention. It is used to further explore CaMKII and provide a basis for better application in the future.

Keywords

Cardiac hypertrophy, CAMK II, CERB, Arrhythmia