Molecular Mechanism of the Effect of Cafestol on Growth Factor-Induced Cardiomyocyte Hypertrophy

Molecular mechanism of the effect of cafestol on growth factor-induced cardiomyocyte hypertrophy. Most of cardiovascular diseases can cause cardiac hypertrophy. Early cardiac hypertrophy can compensate cardiac function, but persistent cardiac hypertrophy would lead to heart failure. In cardiac cells, mechanical stress or endogenous growth factor stimulation can cause cardiac hypertrophy which may cause damage to cardiac function and further lead to heart failure. Endogenous growth factors such as urotensin II (U-II) can cause cardiomyocyte hypertrophy. The applicant’s previous study reported that reactive oxygen species (ROS) may paly a role in signal transduction in cardiomyocytes, and U-II can increase intracellular ROS which is related to cardiomyocyte hypertrophy. Cafestol is a common ingredient in coffee beans. Laboratory studies showed that cafestol has strong anti-oxidant effect and may protect cells from oxidative stress injury. However, the effect of cafestol on U-II-induced cardiomyocyte hypertrophy and its intracellular mechanism(s) remain to be clarified. This project is aimed to study the effects of cafestol on U-II-induced cardiomyocyte hypertrophy and unravel related cellular and molecular mechanisms.