Calpain involved in signal transduction of myocardial remodeling in patients with congestive heart failure / 中华心血管病杂志

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the regulation of calcium sensitive signal substance calpain in signal transduction of myocardial remodeling in patients with congestive heart failure.</p><p><b>METHODS</b>All 39 congestive heart failure (CHF) patients with rheumatic mitral valve stenosis disease were selected and 38 cases of healthy persons were included as controls. Cardiac function parameters were measured by echocardiography. The concentration of angiotension II (AngII) in plasma and myocardial tissues was determined by radio immunoassay (RIA). Western blot was used to assay the protein expression of calpain, cain/cabin 1, cain/cabin 1Delta, and calcineurin (CaN) phosphorylation.</p><p><b>RESULTS</b>The AngII concentrations in the plasma and myocardial tissues in patients with CHF were higher than those in the control group. Meanwhile the AngII concentrations positively correlated to the parameters of the cardiac dilation respectively but negatively correlated to the parameters of cardiac function. Pathological changes of myocardial tissues in CHF with valvular heart disease showed typical myocardial remodeling. The hypertrophy was dominant at early stage of CHF, while at the end stage the characteristics include disordered alignment of the myocytes, the discontinuity and dissolving of cardiomyofibrills, destroyed subcellular organs, and the hyperplasia of interstitial tissue. Compared to the control group, u-calpain, m-calpain, and cain/cabin 1Delta protein expression, CaN phosphorylation in myocardial tissues in CHF groups were highly expressed and their expressions were positively correlated to the severity of CHF. The expression of cain/cabin1 deceased and its expression was negatively correlated to the severity of CHF.</p><p><b>CONCLUSION</b>The degradation of cain/cabin 1 by calpain may play an important role by causing the activation of CaN signal pathway in myocardial remodeling mediated by renin angiotension system in CHF.</p>