Serum amyloid A and atherosclerosis : Current Opinion in Lipidology (original) (raw)
ATHEROSCLEROSIS: CELL BIOLOGY AND LIPOPROTEINS Edited by Andrew Newby and Mohamad Navab
aDepartment of Pathology
bDepartment of Medicine
cBen May Institute for Cancer Biology, University of Chicago, Chicago, Illinois, USA
Correspondence to Godfrey S. Getz, Department of Pathology, The University of Chicago, MC 1089, 5841 S. Maryland Avenue, Chicago, IL 60637, USA. Tel: +1 773 834 4856; fax: +1 773 834 5251; e-mail: [email protected]
Abstract
Purpose of review
Atherosclerosis is a chronic inflammation associated with increased expression of the acute phase isoforms of serum amyloid A (SAA) and in humans is a plasma biomarker for future cardiovascular events. However, whether SAA is only a biomarker or participates in the development of cardiovascular disease is not well characterized. The purpose of this review is to summarize putative functions of SAA relevant to atherogenesis and in-vivo murine studies that directly examine the effect of SAA on atherosclerosis.
Recent findings
Modulation of the expression of SAA1 and/or SAA2 in murine models of atherosclerosis suggests that SAA promotes early atherogenesis. SAA secreted from bone-marrow-derived cells contributes to this antiatherogenic phenotype. SAA also promotes angiotensin-induced abdominal aneurysm in atherogenic mouse models. The reduction in atherosclerosis may be due, at least in part, to remodeling of the acute phase HDL to reduce its capacity to promote cholesterol efflux and reduce its anti-inflammatory ability.
Summary
SAA is more than a marker of cardiovascular disease and is a participant in the early atherogenic process.
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