Endothelial dysfunction and coronary atherosclerosis

Shiro Kitamoto, Kensuke Egashira

Research output: Contribution to journalReview article

12 Citations (Scopus)

Abstract

Increasing evidence has revealed that endothelial cells play an important role in the pathogenesis of development and progression of atherosclerosis. Endothelial dysfunction induces disruption of the balance between vasoconstrictive factors and vasodilatory factors secreted from endothelial cells. Among these factors, NO and angiotensin II are especially important factors, and have been shown to exert various direct effects on the endothelial functions that are closely related to the pathogenesis of atherosclerosis. Endothelial dysfunction induces decreased NO bioactivity and increased angiotensin II expression, which increase oxidative stress and expression of adhesion molecules, cytokines, and chemokines. These conditions mediate inflammation, proliferation, and thrombogenesis in vessel wall and promote atherosclerotic lesions. On the other hand, therapies that improve endothelial dysfunction, such as administration of HMG-CoA reductase inhibitors or angiotensin converting inhibitors, have been demonstrated to reduce cardiovascular events and strokes. In this article, we focus on NO and angiotensin II and describe their roles in the pathogenesis of atherosclerosis.

Original languageEnglish
Pages (from-to)13-22
Number of pages10
JournalCurrent Drug Targets - Cardiovascular and Haematological Disorders
Volume4
Issue number1
DOIs
Publication statusPublished - Mar 1 2004

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Angiotensin II
Coronary Artery Disease
Atherosclerosis
Endothelial Cells
Hydroxymethylglutaryl-CoA Reductase Inhibitors
Angiotensins
Chemokines
Oxidative Stress
Myocardial Infarction
Cytokines
Inflammation
Therapeutics

All Science Journal Classification (ASJC) codes

  • Molecular Medicine
  • Hematology
  • Pharmacology
  • Cardiology and Cardiovascular Medicine

Cite this

Endothelial dysfunction and coronary atherosclerosis. / Kitamoto, Shiro; Egashira, Kensuke.

In: Current Drug Targets - Cardiovascular and Haematological Disorders, Vol. 4, No. 1, 01.03.2004, p. 13-22.

Research output: Contribution to journalReview article

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