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Role of Serum Amyloid A in Atherosclerosis

Overview
Specialty Biochemistry
Date 2019 May 29
PMID 31135596
Citations 34
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Abstract

Purpose Of Review: Acute phase serum amyloid A (SAA) is persistently elevated in chronic inflammatory conditions, and elevated levels predict cardiovascular risk in humans. More recently, murine studies have demonstrated that over-expression of SAA increases and deficiency/suppression of SAA attenuates atherosclerosis. Thus, beyond being a biomarker, SAA appears to play a causal role in atherogenesis. The purpose of this review is to summarize the data supporting SAA as a key player in atherosclerosis development.

Recent Findings: A number of pro-inflammatory and pro-atherogenic activities have been ascribed to SAA. However, the literature is conflicted, as recombinant SAA, and/or lipid-free SAA, used in many of the earlier studies, do not reflect the activity of native human or murine SAA, which exists largely lipid-associated. Recent literatures demonstrate that SAA activates the NLRP3 inflammasome, alters vascular function, affects HDL function, and increases thrombosis. Importantly, SAA activity appears to be regulated by its lipid association, and HDL may serve to sequester and limit SAA activity.

Summary: SAA has many pro-inflammatory and pro-atherogenic activities, is clearly demonstrated to affect atherosclerosis development, and may be a candidate target for clinical trials in cardiovascular diseases.

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References
1.
Kisilevsky R, Manley P . Acute-phase serum amyloid A: perspectives on its physiological and pathological roles. Amyloid. 2012; 19(1):5-14. DOI: 10.3109/13506129.2011.654294. View

2.
Van Eck M, Twisk J, Hoekstra M, Van Rij B, van der Lans C, Bos I . Differential effects of scavenger receptor BI deficiency on lipid metabolism in cells of the arterial wall and in the liver. J Biol Chem. 2003; 278(26):23699-705. DOI: 10.1074/jbc.M211233200. View

3.
Artl A, Marsche G, Lestavel S, Sattler W, Malle E . Role of serum amyloid A during metabolism of acute-phase HDL by macrophages. Arterioscler Thromb Vasc Biol. 2000; 20(3):763-72. DOI: 10.1161/01.atv.20.3.763. View

4.
Fuijkschot W, Morrison M, Zethof I, Krijnen P, Kleemann R, Niessen H . LPS-Induced Systemic Inflammation Does Not Alter Atherosclerotic Plaque Area or Inflammation in APOE3*LEIDEN Mice in the Early Phase Up to 15 Days. Shock. 2017; 50(3):360-365. DOI: 10.1097/SHK.0000000000001026. View

5.
Kotani K, Satoh N, Kato Y, Araki R, Koyama K, Okajima T . A novel oxidized low-density lipoprotein marker, serum amyloid A-LDL, is associated with obesity and the metabolic syndrome. Atherosclerosis. 2008; 204(2):526-31. DOI: 10.1016/j.atherosclerosis.2008.09.017. View