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Autoimmune-mediated oxidative stress and endothelial dysfunction: implications of accelerated vascular injury in type I diabetes. J Surg Res 2009 Jul;155(1):173-8

Date

09/23/2008

Pubmed ID

18805553

DOI

10.1016/j.jss.2008.04.026

Scopus ID

2-s2.0-67349165853   11 Citations

Abstract

The pathogenesis of cardiovascular disease in the setting of type 1 diabetes is not well-defined. The hypothesis that hyperglycemia is largely responsible for vascular endothelial dysfunction, and ultimately atherosclerosis, continues to evolve. However, despite tight glucose control, a subset of patients still develop clinically significant occlusive disease. While the specific mechanisms of persistent vascular injury are not clear, an increasing body of evidence suggests a dysregulated autoimmune response may contribute to the development of vascular injury. That is, the same inflammatory response that is responsible for pancreatic beta-cell destruction may facilitate chronic vascular endothelial injury prior to the onset of hyperglycemia. Herein, we discuss (1) the clinical experience with tight glycemic control and the risk of cardiovascular disease in patients with type 1 diabetes; (2) the cellular mechanisms involved in vascular endothelial injury; and (3) the long-term clinical implications of autoimmune-mediated vascular disease and current treatment strategies.

Author List

Zimmerman MA, Flores SC

Author

Michael A. Zimmerman MD, FACS Professor in the Surgery department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Animals
Atherosclerosis
Autoimmunity
Diabetes Mellitus, Type 1
Diabetic Angiopathies
Endothelium, Vascular
Humans
Hyperglycemia
Inflammation
Oxidative Stress
T-Lymphocytes, Regulatory
jenkins-FCD Prod-486 e3098984f26de787f5ecab75090d0a28e7f4f7c0