Abstract Body: Heart disease ranks first in Western countries and second in developing countries. Both pulmonary heart disease and cardiogenic heart disease produce to cardiac overload, ultimately resulting in pathological myocardial hypertrophy (PCH), causing heart failure and death. PCH is an irreversible, high-risk and common cardiomyopathy, and the incidence rate is increasing. PCH mechanism is complex and remains to be addressed. PCH has characteristics, such as epigenetic regulation disorders.and abnormal increase in protein synthesis. While the biological function of BRF1 and RNA Pol III genes is to determine protein synthesis. Our preliminary studies have shown that drug (ISO) and surgical (TAC) induce myocardial hypertrophy of mice and significantly upregulates the expression of transcription factor BRF1 and its target gene (tRNA and 5S rRNA) transcription, which are positively correlated with experimental myocardial hypertrophy. The high expression of BRF1 and upregulation of tRNA and 5S rRNA transcription have been validated in clinical cases of myocardial hypertrophy as well as. Our previous studies have demonstrated that the abnormally high expression of BRF1 and RNA Pol III genes link to proliferation and rapid growth of cells. Transcription levels of tRNA and 5S rRNA change with the alteration of cellular BRF1 amounts. Alcohol feeding promotes cardiac hypertrophy of animals. Alcohol induces the activation of mitogen and stress-activated protein kinase1 (MSK1), while MSK1 positively modulates BRF1 expression, and tRNA and 5S rRNA transcription. Inhibited MSK1 activity decreases BRF1 expression, and tRNA and 5S rRNA transcription. Interestingly, ISO activates MSK1 in a rat heart cell line. On other hand, knock down BRF1 expression recovers alcohol-induced cardiac hypertrophy. It implies that inhibition of MSK1 may regress PCH, which provides a new direction to develop treatment approaches for the patients of PCH.

*: Corresponding authors; #: Professor Emeritus, University of Southern California.