Simvastatin Attenuates Hypertrophic Responses To Cardiotrophin-1 By JAK-STAT Pathway In Cultured Cardiomyocytes

Left ventricular hypertrophy (LVH) is an independent risk factor for the morbidity and mortality of cardiovascular events in essential hypertension. It was the cardiocytes hypertrophy and phenotype transition from contractile state (adult state) to synthetic state (embryo state) that has been regarded as one of the important pathological bases of LVH. Nevertheless it is an extremely complex physio-physiological process. Meanwhile pathogenesy and effective prevention of LVH have remained to be elucidated completelly. Recent studies documented that proinflammation cytokines were intimately correlate to hypertrophigenesis of cardiocytes, whose specific role and its signal pathway in cardiocytes hypertrophy was become focus. While the cardiotrophin-1 is a new cytokine of the IL-6 family cloned from mouse embryonic stem cell, which is, expressed by cardiocytes, an essential gene to cardiovascular genesis under physiological circumstance. But under patholgical situation, overexpression of the CT-1 is a significant inducer to myocardium reconstitution. The signal pathway of CT-1 is Janus activated kinase/signal transducer activator of transcription (JAK-STAT), which was discovered recant years. JAK-STAT have simple structure with two class signal molecule and has been believed to involved in many physio-physiological process...