Inflammatory mechanisms of diabetic complications

被引：178

作者：

Williams M.D. ^{[1
]}

Nadler J.L. ^{[1
]}

机构：

[1] Division of Endocrinology and Metabolism, University of Virginia, Charlottesville, VA 22908-1405

来源：

Current Diabetes Reports | 2007年 / 7卷 / 3期

基金：

美国国家卫生研究院;

关键词：

Diabetic Nephropathy; Diabetic Retinopathy; Vascular Smooth Muscle Cell; Arterioscler Thromb Vasc Biol; Human Aortic Endothelial Cell;

D O I：

10.1007/s11892-007-0038-y

中图分类号：

学科分类号：

摘要：

Activation of inflammatory process may contribute to the development of type 2 diabetes mellitus. In addition, inflammation appears to be a major mechanism responsible for vascular damage leading to the clinically well-recognized complications of diabetes. Inflammation cytokine and chemokine mediators released from visceral fat contribute to atherosclerosis plaque formation and increased risk for myocardial infarction and stroke. Activation of growth factors and adhesion molecules may promote the movement of inflammatory cells into the renal microvasculature, predisposing to the development of diabetic nephropathy. Emerging evidence also indicates that markers of inflammation are associated with the more severe forms of diabetic retinopathy. Future approaches to the treatment of diabetic complications may involve regulation of inflammatory processes, specifically targeting factors that contribute to vascular damage. Copyright © 2007 by Current Medicine Group LLC.

引用

页码：242 / 248

页数：6

共 69 条

[41]

Nadler J.L., Pei H., Bevard M., Bruce A., Reduced macrophage infiltration in visceral adipose tissue of 12-Lipoxygenase knockout mice, Paper presented at the Arteriosclerosis, Thrombosis and Vascular Biology Annual Conference 2007, (2007)

[42]

Wen Y., Gu J., Chakrabarti S.K., Et al., The role of 12/15-lipoxygenase in the expression of IL-6 and TNF-alpha in macrophages, Endocrinology, 148, pp. 1313-1322, (2007)

[43]

Finne P., Reunanen A., Stenman S., Et al., Incidence of end-stage renal disease in patients with type 1 diabetes, JAMA, 294, pp. 1782-1787, (2005)

[44]

Hohenstein B., Hausknecht B., Boehmer K., Et al., Local VEGF activity but not VEGF expression is tightly regulated during diabetic nephropathy in man, Kidney Int, 69, pp. 1654-1661, (2006)

[45]

Jandeleit-Dahm K., Cooper M., Hypertension and diabetes: Role of the renin-angiotensin system, Endocrinol Metab Clin North Am, 35, pp. 469-490, (2006)

[46]

Xu S., Jiang B., Maitland K.A., Et al., The thromboxane receptor antagonist S18886 attenuates renal oxidant stress and proteinuria in diabetic apolipoprotein E-deficient mice, Diabetes, 55, pp. 110-119, (2006)

[47]

Gomez-Garre D., Largo R., Tejera N., Et al., Activation of NF-kappaB in tubular epithelial cells of rats with intense proteinuria: Role of angiotensin II and endothelin-1, Hypertension, 37, pp. 1171-1178, (2001)

[48]

Mezzano S., Aros C., Droguett A., Et al., NF-kappa B activation and overexpression of regulated genes in human diabetic nephropathy, Nephrol Dial Transplant, 19, pp. 2505-2512, (2004)

[49]

Banba N., Nakamura T., Matsumura M., Et al., Possible relationship of monocyte chemoattractant protein-1 with diabetic nephropathy, Kidney Int, 58, pp. 684-690, (2000)

[50]

Young B., Johnson R., Alpers C., Et al., Cellular events in the evolution of experimental diabetic nephropathy, Kidney Int, 47, pp. 935-944, (1995)

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