Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1982 Apr 15;126(8):903-8.

Smooth muscle and endothelial cell function in the pathogenesis of atherosclerosis

Smooth muscle and endothelial cell function in the pathogenesis of atherosclerosis

A I Gotlieb. Can Med Assoc J. .

Abstract

Although clinical studies have been very useful in identifying factors that accelerate the development of atherosclerotic vascular disease, the pathogenesis of the vascular lesions remains unknown. Studies carried out in the last 10 years have shown that smooth muscle and endothelial cells of the vascular wall play a very important role in atherogenesis. It has become apparent that these cells are very active metabolically during the initiation and subsequent growth of the plaques, and that the materials that these cells produce and secrete are important in the composition and growth of the plaques. In addition, there are important interactions at the vessel wall-blood interface that involve endothelial cells, hemodynamic forces and many constituents of the blood, including platelets, lipoproteins, coagulation factors, fibrinolytic agents and leukocytes. In this article the numerous functions of both smooth muscle and endothelial cells are discussed and the effects of known atherogenic agents on these cellular functions are reviewed. Emphasis is placed on the important interactions that take place both within the vessel wall and at the vessel wall-blood interface. Understanding of the regulation of smooth muscle and endothelial cell function during the development and subsequent growth of fibrofatty plaques may be useful in designing appropriate therapeutic interventions to control atherosclerotic disease.

PubMed Disclaimer

References

    1. N Engl J Med. 1969 Jul 17;281(3):115-9 - PubMed
    1. J Clin Invest. 1971 Aug;50(8):1666-77 - PubMed
    1. Proc Natl Acad Sci U S A. 1974 May;71(5):1906-9 - PubMed
    1. Circ Res. 1975 Feb;36(2):319-27 - PubMed
    1. Lab Invest. 1975 Mar;32(3):339-51 - PubMed

Publication types

MeSH terms

LinkOut - more resources