Published in Obesity and Diabetes Week, January 3rd, 2005
According to researchers from England, "We previously demonstrated that chronic stimulation of the beta2 -adrenergic receptor (beta2 -AR) increases proliferation of cultured human cardiac fibroblasts (CF) via an autocrine mechanism. [Now we have} investigated the role of endothelin-1 (ET-1) in this process. ETA-receptor antagonism or protein kinase C inhibition abolished the beta2 -AR-induced increase in cell proliferation."
N.A. Turner and colleagues of the University of Leeds reported,...
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