Journal
BIOMOLECULES
Volume 11, Issue 12, Pages -Publisher
MDPI
DOI: 10.3390/biom11121883
Keywords
cardiovascular disease; abdominal aortic aneurysm; serum amyloid A; HDL
Categories
Funding
- National Institutes of Health [R01 HL147381]
- Department of Veterans Affairs [BX004275]
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Epidemiological data show a positive correlation between serum amyloid A (SAA) levels and cardiovascular disease severity and mortality. Animal studies suggest a causal role for SAA in atherosclerosis development. In mice, suppressing SAA has been shown to reduce abdominal aortic aneurysm formation. Researchers aim to understand the pathway of SAA involvement in order to consider it as a therapeutic target for cardiovascular diseases.
Epidemiological data positively correlate plasma serum amyloid A (SAA) levels with cardiovascular disease severity and mortality. Studies by several investigators have indicated a causal role for SAA in the development of atherosclerosis in animal models. Suppression of SAA attenuates the development of angiotensin II (AngII)-induced abdominal aortic aneurysm (AAA) formation in mice. Thus, SAA is not just a marker for cardiovascular disease (CVD) development, but it is a key player. However, to consider SAA as a therapeutic target for these diseases, the pathway leading to its involvement needs to be understood. This review provides a brief description of the pathobiological significance of this enigmatic molecule. The purpose of this review is to summarize the data relevant to its role in the development of CVD, the pitfalls in SAA research, and unanswered questions in the field.
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