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Cardiovascular Research Advance Access [Accepted Manuscript] published online on April 22, 2008
Cardiovascular Research, doi:10.1093/cvr/cvn099
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

Early atherosclerosis in humans: Role of diffuse intimal thickening and extracellular matrix proteoglycans

Yutaka Nakashima1, Thomas N. Wight2 and Katsuo Sueishi3

1 Division of Pathology, Fukuoka Red Cross Hospital, 3-1-1 Ogusu, Minami-ku, Fukuoka 815-8555, Japan
2 The Hope Heart Program at Benaroya Research Institute and the University of Washington, 1201 Ninth Ave, Seattle, WA98101, U.S.A
3 Pathophysiological and Experimental Pathology, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan

Corresponding author: Yutaka Nakashima, M.D., Ph.D. Division of Pathology Fukuoka Red Cross Hospital 3-1-1 Ogusu, Minami-ku Fukuoka 815-8555 Japan Tel: +81-92-521-1211 Fax: +81-92-533-9960 E-mail: y-nakashima{at}fukuoka-med.jrc.or.jp

This review attempts to define the early events that lead to lesions of human atherosclerosis based on careful morphological studies in human autopsy specimens. In contrast to most small laboratory animals, diffuse intimal thickening (DIT) is present in human arteries before atherosclerosis develops, particularly in the atherosclerosis-prone arteries such as coronary arteries and abdominal aorta. In the earliest stage of atherosclerosis, lipids deposit eccentrically in the deep layer of DIT to form Type I lesions. These layers are enriched in extracellular matrix proteoglycans such as biglycan. Following lipid deposition, macrophages appear in these regions and foam cells are observed (Type II lesions). Such observations support the "response-to-retention" hypothesis that states that a principle early event in the pathogenesis of human atherosclerosis is the trapping and retention of lipoproteins by extracellular matrix proteoglycans followed by infiltration and accumulation of macrophages.

KEYWORDS arteries; human; early atherosclerosis; proteoglycans, lipoproteins

Time for primary review: 34 days

Classifications: vasculature, organ, pathophysiology, aging, arteries, atherosclerosis, extracellular matrix, lipoproteins


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