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Updated: Aug 11, 2026
05:48
Rapid Generation of Amyloid from Native Proteins In vitro
Published on: December 5, 2013
Serum amyloid A: the "other" inflammatory protein
1Division of Cardiology, University of Washington, Seattle 98195-6422, USA. cardiac@u.washington.edu
Current Atherosclerosis Reports
|February 4, 2006
Summary
Serum amyloid A (SAA) is an inflammatory protein linked to atherosclerosis. This review explores SAA
Area of Science:
- Biochemistry
- Immunology
- Cardiovascular Science
Background:
- Inflammation is a known hallmark of atherosclerotic lesions.
- Chronic low-level elevations of plasma inflammatory proteins like C-reactive protein (CRP) and serum amyloid A (SAA) are increasingly recognized.
- These proteins may act as atherosclerosis risk markers and actively participate in atherogenesis.
Purpose of the Study:
- To review the evidence for and against the roles of CRP in atherosclerosis.
- To focus on the role of SAA in atherogenesis, including its regulation and function.
- To explore SAA's potential as a mediator linking inflammation, dyslipidemia, obesity, and insulin resistance to atherosclerosis.
Main Methods:
- Literature review of existing studies on CRP and SAA.
- Analysis of data concerning SAA regulation by dietary cholesterol, obesity, and insulin resistance.
- Examination of SAA's interaction with high-density lipoprotein (HDL).
Main Results:
- Evidence for CRP's role as an atherosclerosis risk marker and in atherogenesis is reviewed.
- SAA is an inflammatory protein associated with high-density lipoprotein (HDL), potentially altering its function.
- SAA's regulation is influenced by dietary cholesterol, obesity, and insulin resistance.
Conclusions:
- SAA may play a critical role in mediating the contributions of inflammation, dyslipidemia, obesity, and insulin resistance to atherogenesis.
- SAA's position at the intersection of these risk factors highlights its significance in cardiovascular disease development.
- Further research into SAA's mechanisms is warranted to understand its full impact on atherosclerosis.
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