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Pathological Remodeling of Myocardium in Spontaneous Hypertensive Rats with Experimental Diabetes Mellitus: Role of Mitochondrial Dysfunction

机译:实验性糖尿病自发性高血压大鼠心肌的病理重塑:线粒体功能障碍的作用

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摘要

The expression of cardiotrophin-1, annexin V, titin and type I collagen was investigated in the myocardium of normotensive Wistar rats and spontaneous hypertensive rats with experimental diabetes and without it. The Ca~(2+) -induced mitochondrial permeability transition pore was assessed in the mitochondria isolated from rat hearts. The content of cardiotrophin-1, annexin V and type I collagen in spontaneous hypertensive rats with diabetes was higher compared to normotensive and diabetic rats. The cardiac titin level was 27% lower in animals with hypertension and diabetes compared with spontaneous hypertensive rats without diabetes. The changes in cardiotrophin-1, annexin V, titin and type I collagen expression were associated with higher sensitivity of mitochondrial pore to Ca~(2+) in the myocardium of spontaneous hypertensive rats with diabetes mellitus.
机译:研究了正常血压的Wistar大鼠和自发性高血压大鼠的心肌中心肌营养因子-1,膜联蛋白V,纤溶蛋白和I型胶原的表达。在从大鼠心脏分离的线粒体中评估了Ca〜(2+)诱导的线粒体通透性过渡孔。自发性高血压糖尿病大鼠的心肌营养因子-1,膜联蛋白V和I型胶原的含量高于正常血压和糖尿病大鼠。与没有糖尿病的自发性高血压大鼠相比,患有高血压和糖尿病的动物的心脏肌酐水平降低了27%。糖尿病自发性高血压大鼠心肌中心肌营养因子-1,膜联蛋白V,肌钙蛋白和I型胶原表达的变化与线粒体孔对Ca〜(2+)的敏感性较高有关。

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