A role for decorin in the remodeling of myocardial infarction

摘要: Because the small leucine-rich proteoglycan decorin has been implicated in regulation of collagen fibrillogenesis leading to proper extracellular matrix assembly, we hypothesized it could play a key role cardiac fibrosis following myocardial infarction. In this study ligated left anterior descending coronary artery wildtype and decorin-null mice produce large infarcts wall ventricle. At early stages post-coronary occlusion infarction size did not appreciably differ between two genotypes. However, found wider distribution fibril sizes with less organization loose packing mature scar from mice. Thus, tested hypothesis that these abnormal fibrils would adversely affect post-infarction mechanics ventricular remodeling. Indeed, size, right remote hypertrophy, dilatation were greater animals compared littermates 14 days after acute Echocardiography revealed depressed systolic function 4 8 weeks post-ischemia animals. These changes indicate is required for fibrotic evolution infarctions, its absence leads tissue formation. This might contribute aneurysmal dilatation, function.