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心肌内皮细胞可能通过释放生长因子,促进心肌细胞肥大。然而,这些因子在很大程度上仍然是未知的,研究人员假设分泌的C1q-肿瘤坏死因子相关蛋白9(C1q-tumor necrosis factor-related protein-9,CTRP9)可能作为压力超负荷时调节心脏重塑的内皮衍生蛋白。该研究的目的为检测心脏CTRP9的来源及其在压力超负荷期间的功能。方法和结果:CTRP9主要来源于心肌毛细血管内皮细胞。在肥大的人体心脏中和
Myocardial endothelial cells may promote cardiomyocyte hypertrophy by releasing growth factors. However, to a large extent these factors are still unknown and the researchers hypothesized that the secreted C1q-tumor necrosis factor-related protein-9 (CTRP9) may regulate heart weight as stress overload Plastic endothelial derivatives. The purpose of this study was to examine the origin of cardiac CTRP9 and its function during stress overload. Methods and Results: CTRP9 mainly derived from cardiac capillary endothelial cells. In hypertrophic human heart and