Role of serum amyloid A in atherosclerosis

Research output: Contribution to journalReview articlepeer-review

47 Scopus citations

Abstract

Purpose of reviewAcute 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 findingsA 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.SummarySAA 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.

Original languageEnglish
Pages (from-to)320-325
Number of pages6
JournalCurrent Opinion in Lipidology
Volume30
Issue number4
DOIs
StatePublished - Aug 1 2019

Bibliographical note

Publisher Copyright:
© 2019 Lippincott Williams and Wilkins. All rights reserved.

Keywords

  • HDL
  • atherosclerosis
  • cardiovascular disease
  • inflammation
  • serum amyloid A
  • vascular

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Molecular Biology
  • Genetics
  • Nutrition and Dietetics
  • Cardiology and Cardiovascular Medicine
  • Cell Biology

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