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Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein
Published on: October 12, 2017
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Serum amyloid A and atherosclerosis.
Godfrey S Getz1, Paulette A Krishack, Catherine A Reardon
1aDepartment of Pathology bDepartment of Medicine cBen May Institute for Cancer Biology, University of Chicago, Chicago, Illinois, USA.
Current Opinion in Lipidology
|September 1, 2016
Summary
Serum amyloid A (SAA) is a key player in atherosclerosis development, not just a biomarker. Studies show SAA promotes early atherogenesis and abdominal aortic aneurysms in mice.
Area of Science:
- Cardiovascular Science
- Inflammation Research
- Biomarker Discovery
Background:
- Atherosclerosis is a chronic inflammatory disease linked to elevated serum amyloid A (SAA) isoforms.
- SAA is a known plasma biomarker for cardiovascular events.
- The precise role of SAA in cardiovascular disease development requires further elucidation.
Purpose of the Study:
- To review the proposed functions of SAA in atherogenesis.
- To summarize in-vivo murine studies investigating SAA's impact on atherosclerosis.
Main Methods:
- Analysis of murine models with modulated SAA1/SAA2 expression.
- Investigation of SAA's role in angiotensin-induced abdominal aortic aneurysm models.
- Assessment of HDL remodeling in response to SAA.
Main Results:
- Murine studies suggest SAA promotes early atherogenesis.
- SAA secreted by bone-marrow-derived cells contributes to an anti-atherogenic phenotype.
- SAA exacerbates angiotensin-induced abdominal aortic aneurysms in mice.
- Acute phase HDL remodeling may reduce cholesterol efflux and anti-inflammatory capacity.
Conclusions:
- Serum amyloid A (SAA) actively participates in the early stages of atherogenesis.
- SAA is more than a biomarker; it is a contributing factor to cardiovascular disease progression.
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