Nancy R Webb1. 1. Department of Pharmacology and Nutritional Sciences, Saha Cardiovascular Research Center, and Barnstable Brown Diabetes Center, University of Kentucky, 553 Wethington Building, 900 South Limestone, Lexington, KY, 40536-0200, USA. nrwebb1@uky.edu.
Abstract
PURPOSE OF REVIEW: Serum amyloid A (SAA) is a highly sensitive acute phase reactant that has been linked to a number of chronic inflammatory diseases. During a systemic inflammatory response, liver-derived SAA is primarily found on high-density lipoprotein (HDL). The purpose of this review is to discuss recent literature addressing the pathophysiological functions of SAA and the significance of its association with HDL. RECENT FINDINGS: Studies in gene-targeted mice establish that SAA contributes to atherosclerosis and some metastatic cancers. Accumulating evidence indicates that the lipidation state of SAA profoundly affects its bioactivities, with lipid-poor, but not HDL-associated, SAA capable of inducing inflammatory responses in vitro and in vivo. Factors that modulate the equilibrium between lipid-free and HDL-associated SAA have been identified. HDL may serve to limit SAA's bioactivities in vivo. Understanding the factors leading to the release of systemic SAA from HDL may provide insights into chronic disease mechanisms.
PURPOSE OF REVIEW: Serum amyloid A (SAA) is a highly sensitive acute phase reactant that has been linked to a number of chronic inflammatory diseases. During a systemic inflammatory response, liver-derived SAA is primarily found on high-density lipoprotein (HDL). The purpose of this review is to discuss recent literature addressing the pathophysiological functions of SAA and the significance of its association with HDL. RECENT FINDINGS: Studies in gene-targeted mice establish that SAA contributes to atherosclerosis and some metastatic cancers. Accumulating evidence indicates that the lipidation state of SAA profoundly affects its bioactivities, with lipid-poor, but not HDL-associated, SAA capable of inducing inflammatory responses in vitro and in vivo. Factors that modulate the equilibrium between lipid-free and HDL-associated SAA have been identified. HDL may serve to limit SAA's bioactivities in vivo. Understanding the factors leading to the release of systemic SAA from HDL may provide insights into chronic disease mechanisms.
Authors: Mieke De Buck; Mieke Gouwy; Ji Ming Wang; Jacques Van Snick; Paul Proost; Sofie Struyf; Jo Van Damme Journal: Cytokine Growth Factor Rev Date: 2015-12-28 Impact factor: 7.638
Authors: Ailing Ji; Andrea C Trumbauer; Victoria P Noffsinger; Hayce Jeon; Avery C Patrick; Frederick C De Beer; Nancy R Webb; Lisa R Tannock; Preetha Shridas Journal: PLoS One Date: 2022-04-18 Impact factor: 3.752