Abstract: Objective To investigate the roles and mechanism of HECT and RLD domain containing E3 ubiquitin protein ligase 2（HERC2） in cardiac hypertrophy.
Methods The expression of hypertrophic genes and HERC2 were analyzed in the myocardial tissues from patients with hypertrophic cardiomyopathy and the controls by quantitative reverse transcription-polymerase chain reaction(qRT-PCR). Cardiac hypertrophy was induced in rat with angiotensin Ⅱ, and the expression of hypertrophic genes and HERC2 was analyzed. siRNA was used to knock down HERC2 in cardiomyocytes and cardiomyocyte hypertrophy was induced with angiotensin Ⅱ. Then, the cardiomyocyte size, expression of hypertrophic genes and activation of the phosphatidylinositol 3-kinase/AKT serine/threonine kinase(PI3K-AKT) signaling were analyzed.
Results The expressions of HERC2 were significantly upregulated in the myocardial tissues of patients with hypertrophic cardiomyopathy compared with the controls. The overexpression of HERC2 was also observed in rat cardiac hypertrophy induced by angiotensin Ⅱ. Knockdown of HERC2 with siRNA repressed angiotensin Ⅱ-induced increase in cardiomyocyte size and expression of hypertrophic genes natriuretic peptide A, natriuretic peptide B and myosin heavy chain 7.
Conclusion HERC2 is highly expressed in the process of cardiac hypertrophy. HERC2 can promote cardiac hypertrophy by regulating PI3K-Akt signaling pathway.

Key words: cardiomyopathy, hypertrophic, angiotensin Ⅱ, phosphatidylinositol 3-Kinase