A review of endothelial dysfunction in diabetes: A focus on the contribution of a dysfunctional eNOS

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60 Citations (Scopus)

Abstract

Although the etiology of vascular dysfunction in diabetes has been extensively investigated in both humans as well as animal models of human diabetes, the relative importance of the cellular pathways involved is still not fully understood. In this review, we focus on reviewing the literature that provides insights into how an acute exposure to hyperglycemia results in a dysregulation of endothelial nitric oxide synthase function, the subsequent downstream effects of endothelial nitric oxide synthase dysregulation, and the development of endothelial dysfunction.

Original languageEnglish
Pages (from-to)102-115
Number of pages14
JournalJournal of the American Society of Hypertension
Volume4
Issue number3
DOIs
Publication statusPublished - May 2010

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Nitric Oxide Synthase Type III
Hyperglycemia
Blood Vessels
Animal Models

Keywords

  • apoptosis
  • calpain
  • cyclooxygenase (COX)
  • Diabetes
  • endothelial nitric oxide synthase (eNOS)
  • endothelium-derived contracting factor (EDCFs)
  • endothelium-derived hyperpolarizing factor (EDHF)
  • histone methylation
  • hyperglycemia
  • NADPH oxidase
  • protein kinase C (PKC)
  • store-operated Ca2+ entry (SOCE)

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Internal Medicine

Cite this

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abstract = "Although the etiology of vascular dysfunction in diabetes has been extensively investigated in both humans as well as animal models of human diabetes, the relative importance of the cellular pathways involved is still not fully understood. In this review, we focus on reviewing the literature that provides insights into how an acute exposure to hyperglycemia results in a dysregulation of endothelial nitric oxide synthase function, the subsequent downstream effects of endothelial nitric oxide synthase dysregulation, and the development of endothelial dysfunction.",
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