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2 型糖尿病引起的内皮功能障碍的潜在致病炎症机制。

Potential pathogenic inflammatory mechanisms of endothelial dysfunction induced by type 2 diabetes mellitus.

机构信息

1st Cardiology Unit, Hippokration Hospital, Athens University Medical School, Athens, Greece.

出版信息

Curr Pharm Des. 2011 Dec;17(37):4147-58. doi: 10.2174/138161211798764825.

DOI:10.2174/138161211798764825
PMID:22204375
Abstract

Insulin resistance and the vascular complications of diabetes include activation of the inflammation cascade, endothelial dysfunction, and oxidative stress. The comorbidities of diabetes, namely obesity, insulin resistance, hyperglycemia, hypertension and dyslipidemia collectively aggravate these processes while antihyperglycemic interventions tend to correct them. Increased C-reactive protein, interleukin 6, tumor necrosis factor alpha and especially interstitial cellular adhesion molecule-1, vascular cellular adhesion molecule-1, and E-selectin are associated with cardiovascular and non-cardiovascular complications of both type 1 and type 2 diabetes. We sought to review the clinical implications of the inflammation theory, including the relevance of inflammation markers as predictors of type 2 diabetes in clinical studies, and the potential treatments of diabetes, inferred from the pathophysiology.

摘要

胰岛素抵抗和糖尿病的血管并发症包括炎症级联的激活、内皮功能障碍和氧化应激。糖尿病的合并症,即肥胖、胰岛素抵抗、高血糖、高血压和血脂异常,共同加重了这些过程,而抗高血糖干预则倾向于纠正这些过程。C 反应蛋白、白细胞介素 6、肿瘤坏死因子-α,尤其是细胞间黏附分子-1、血管细胞黏附分子-1 和 E-选择素的增加与 1 型和 2 型糖尿病的心血管和非心血管并发症有关。我们试图综述炎症理论的临床意义,包括炎症标志物作为预测 2 型糖尿病的临床研究中的相关性,以及从病理生理学推断出的糖尿病的潜在治疗方法。

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