Abstract

The novel idea that the molecular regulation of cardiac hypertrophy is closely related to tumour/cancer growth has emerged recently. One key finding was the identification of tumour suppressor RASSF1A as a powerful inhibitor of pathological hypertrophy. The mammalian STE20-like kinase 2 (Mst2) forms a molecular complex with RASSF1A and is also implicated in the development of various tumours. In contrast to Mst1, the role of Mst2 in the heart has not been precisely elucidated. We used Mst2 knockout mice and isolated neonatal rat cardiomyocytes (NRCM) with an adenoviral mediated overexpression of Mst2 to investigate the role of Mst2 in the heart. Mst2-/- mice exhibited a significant reduction of hypertrophy in response to transverse aortic constriction (30% elevation in heart weight/tibia length ratio in Mst2-/- mice compared to 50% in wild type (WT), n=8, P

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