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

[51]

Chow F., Ozols E., Nikolic-Paterson D.J., Et al., Macrophages in mouse type 2 diabetic nephropathy: Correlation with diabetic state and progressive renal injury, Kidney Int, 65, pp. 116-128, (2004)

[52]

Coimbra T.M., Janssen U., Grone H.J., Et al., Early events leading to renal injury in obese Zucker (fatty) rats with type II diabetes, Kidney Int, 57, pp. 167-182, (2000)

[53]

Park C.W., Kim J.H., Lee J.W., Et al., High glucose-induced intercellular adhesion molecule-1 (ICAM-1) expression through an osmotic effect in rat mesangial cells is PKC-NF-kappaB-dependent, Diabetologia, 43, pp. 1544-1553, (2000)

[54]

Okouchi M., Okayama N., Shimizu M., Et al., High insulin exacerbates neutrophil-endothelial cell adhesion through endothelial surface expression of intercellular adhesion molecule-1 via activation of protein kinase C and mitogen-activated protein kinase, Diabetologia, 45, pp. 556-559, (2002)

[55]

Yokoyama H., Takaeda M., Wada T., Et al., Glomerular ICAM-1 expression related to circulating TNF-alpha in human glomerulonephritis, Nephron, 76, pp. 425-433, (1997)

[56]

Chow F.Y., Nikolic-Paterson D.J., Ozols E., Et al., Intercellular adhesion molecule-1 deficiency is protective against nephropathy in type 2 diabetic db/db mice, J Am Soc Nephrol, 16, pp. 1711-1722, (2005)

[57]

Congdon N.G., Friedman D.S., Lietman T., Important causes of visual impairment in the world today, JAMA, 290, pp. 2057-2060, (2003)

[58]

Frank R.N., Diabetic retinopathy, N Engl J Med, 350, pp. 48-58, (2004)

[59]

Nguyen T.T., Wong T.Y., Retinal vascular manifestations of metabolic disorders, Trends Endocrinol Metab, 17, pp. 262-268, (2006)

[60]

Orchard T.J., Dorman J.S., Maser R.E., Et al., Prevalence of complications in IDDM by sex and duration. Pittsburgh Epidemiology of Diabetes Complications Study II, Diabetes, 39, pp. 1116-1124, (1990)

← 1 2 3 4 5 6 7 →