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CIDEC:糖尿病血管炎症中的一个潜在因素。

CIDEC: A Potential Factor in Diabetic Vascular Inflammation.

作者信息

Song Fang-Qiang, Zhou Hui-Min, Ma Wei-Xuan, Li Yu-Lin, Hu Bo-Ang, Shang Yuan-Yuan, Wang Zhi-Hao, Zhong Ming, Zhang Wei, Ti Yun

机构信息

The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.

Department of Critical Care Medicine, Tengzhou Central People's Hospital, Tengzhou, China.

出版信息

J Vasc Res. 2022;59(2):114-123. doi: 10.1159/000520685. Epub 2022 Feb 4.

Abstract

Cell death-inducing DFF45-like effector C (CIDEC) is involved in diet-induced adipose inflammation. Whether CIDEC plays a role in diabetic vascular inflammation remains unclear. A type 2 diabetic rat model was induced by high-fat diet and low-dose streptozotocin. We evaluated its characteristics by metabolic tests, Western blot analysis of CIDEC and C1q/tumor necrosis factor-related protein-3 (CTRP3) expression, and histopathological analysis of aortic tissues. The diabetic group exhibited elevated CIDEC expression, aortic inflammation, and remodeling. To further investigate the role of CIDEC in the pathogenesis of aortic inflammation, gene silencing was used. With CIDEC gene silencing, CTRP3 expression was restored, accompanied with amelioration of insulin resistance, aortic inflammation, and remodeling in diabetic rats. Thus, the silencing of CIDEC is potent in mediating the reversal of aortic inflammation and remodeling, indicating that CIDEC may be a potential therapeutic target for vascular complications in diabetes.

摘要

细胞死亡诱导DFF45样效应因子C(CIDEC)参与饮食诱导的脂肪炎症。CIDEC是否在糖尿病血管炎症中起作用仍不清楚。通过高脂饮食和低剂量链脲佐菌素诱导建立2型糖尿病大鼠模型。我们通过代谢测试、CIDEC和C1q/肿瘤坏死因子相关蛋白-3(CTRP3)表达的蛋白质印迹分析以及主动脉组织的组织病理学分析来评估其特征。糖尿病组表现出CIDEC表达升高、主动脉炎症和重塑。为了进一步研究CIDEC在主动脉炎症发病机制中的作用,采用了基因沉默方法。随着CIDEC基因沉默,CTRP3表达得以恢复,同时糖尿病大鼠的胰岛素抵抗、主动脉炎症和重塑得到改善。因此,CIDEC的沉默在介导主动脉炎症和重塑的逆转方面具有强大作用,表明CIDEC可能是糖尿病血管并发症的潜在治疗靶点。

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