Endothelial Dysfunction, Inflammation, and Apoptosis in Diabetes Mellitus

被引：271

作者：

van den Oever, Inge A. M. ^{[2
]}

Raterman, Hennie G. ^{[3
]}

Nurmohamed, Mike T. ^{[1
,2
]}

Simsek, Suat ^{[1
,4
]}

机构：

[1] Vrije Univ Amsterdam Med Ctr, Dept Internal Med, Amsterdam, Netherlands

[2] Jan van Breemen Inst, Dept Rheumatol, Amsterdam, Netherlands

[3] Vrije Univ Amsterdam Med Ctr, Dept Rheumatol, Amsterdam, Netherlands

[4] Med Ctr Alkmaar, Dept Internal Med, NL-1815 JD Alkmaar, Netherlands

来源：

MEDIATORS OF INFLAMMATION | 2010年 / 2010卷

关键词：

C-REACTIVE PROTEIN; VASCULAR SUPEROXIDE-PRODUCTION; DECREASES ENOS EXPRESSION; GLUCOSE-INDUCED APOPTOSIS; JUN NH2-TERMINAL KINASE; GLYCATION END-PRODUCTS; NITRIC-OXIDE SYNTHASE; NF-KAPPA-B; CELL APOPTOSIS; INSULIN-RESISTANCE;

D O I：

10.1155/2010/792393

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Endothelial dysfunction is regarded as an important factor in the pathogenesis of vascular disease in obesity-related type 2 diabetes. The imbalance in repair and injury (hyperglycemia, hypertension, dyslipidemia) results in microvascular changes, including apoptosis of microvascular cells, ultimately leading to diabetes related complications. This review summarizes the mechanisms by which the interplay between endothelial dysfunction, inflammation, and apoptosis may cause ( micro) vascular damage in patients with diabetes mellitus.

引用

页数：15

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