PDF(Pubmed)
Abstract：
Patients with chronic kidney disease (CKD) face a high risk of cardiovascular disease. Previous studies reported that endogenous thrombospondin 1 (TSP1) involves right ventricular remodeling and dysfunction. Here we show that a murine model of CKD increased myocardial TSP1 expression and produced left ventricular hypertrophy, fibrosis, and dysfunction. TSP1 knockout mice were protected from these features. In vitro, indoxyl sulfate is driving deleterious changes in cardiomyocyte through the TSP1. In patients with CKD, TSP1 and aryl hydrocarbon receptor were both differentially expressed in the myocardium. Our findings summon large clinical studies to confirm the translational role of TSP1 in patients with CKD.
摘要：
慢性肾脏病（CKD）患者面临心血管疾病的高风险。先前的研究报道内源性血小板反应蛋白1（TSP1）涉及右心室重构和功能障碍。在这里，我们显示CKD的小鼠模型增加心肌TSP1表达并产生左心室肥厚，纤维化，和功能障碍。保护TSP1敲除小鼠免受这些特征的影响。体外，硫酸吲哚酚通过TSP1驱动心肌细胞的有害变化。在CKD患者中，TSP1和芳烃受体均在心肌中差异表达。我们的发现召唤大型临床研究来证实TSP1在CKD患者中的转化作用。
