activation: enhanced cell cycle progression and reduced myofibro-blast content in diabetic myocardium. Am J Physiol Endocrinol Metab 297: E1147–E1153, 2009. First published August 25, 2009; doi:10.1152/ajpendo.00327.2009.—Diabetic patients are prone to de-veloping myocardial fibrosis and suffer from decreased wound heal-ing capabilities. The purpose of this study was to determine whether diabetes alters cardiac fibroblast activity in the myocardium in a 6-wk streptozotocin-induced type 1 diabetic model. In vivo echocardiogra-phy indicated significant dilation of the left ventricle (LV) in the diabetic animals, while cardiac function was comparable to that in the normal group. We isolated cardiac fibroblasts from diabetic and control hearts and observed increased proliferation of the diabetic fibroblasts. Microarray analysis using mRNA collected from whole LVs revealed downregulation of known inhibitors of proliferation, p53 and p21, in the diabetic group, consistent with our proliferatio
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