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Cardiovascular Research 1999 41(2):376-384; doi:10.1016/S0008-6363(98)00321-6
© 1999 by European Society of Cardiology
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Copyright © 1999, European Society of Cardiology

Collagen synthesis in atherosclerosis: too much and not enough

Mark D. Rekhter*

Department of Cardiovascular Therapeutics, Parke-Davis Pharmaceutical Research Division, Warner-Lambert Company, 2800 Plymouth Road, Ann Arbor, MI 48105, USA

* Tel.: +1-734-622-2970; fax: +1-734-722-1480; e-mail: mark.rekhter @wl.com

Fibrillar collagen is a critical component of atherosclerotic lesions. Uncontrolled collagen accumulation leads to arterial stenosis, while excessive collagen breakdown combined with inadequate synthesis weakens plaques thereby making them prone to rupture. This review discusses cellular sources of collagen synthesis in atherosclerosis, local and systemic factors modulating collagen gene expression, as well as temporal and spatial patterns of collagen production in human and experimental atherosclerotic lesions.

KEYWORDS Atherosclerosis; Restenosis; Collagen; Gene expression; Plaque rupture


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