ArticleJournal of the American Heart Association2015
Serum Amyloid A Facilitates Early Lesion Development in Ldlr-/- Mice.
Article in Journal of the American Heart Association, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
- Serum amyloid A in HFpEF and cardiometabolic diseases.Basic research in cardiology · 2026Review
- Serum amyloid A in the oral microenvironment: implications for inflammation, host-microbe interactions, and disease monitoring.Frontiers in immunology · 2026Review
- Serum amyloid A: multifaceted roles in inflammation and cellular interactions.Immunologic research · 2025Review
- Comprehensive analysis of heterogeneity and cell-cell interactions in Crohn's disease reveals novel location-specific insights.Journal of advanced research · 2025Article
- Lactobacillus Intestinalis Primes Epithelial Cells to Suppress Colitis-Related Th17 Response by Host-Microbe Retinoic Acid Biosynthesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Serum amyloid A and metabolic disease: evidence for a critical role in chronic inflammatory conditions.Frontiers in cardiovascular medicine · 2023Review
- Review
- Role of Serum Amyloid A in Abdominal Aortic Aneurysm and Related Cardiovascular Diseases.Biomolecules · 2021Review
- New insights into the emerging effects of inflammatory response on HDL particles structure and function.Molecular biology reports · 2021Review
- Review
- Sexually Dimorphic Relationships Among Saa3 (Serum Amyloid A3), Inflammation, and Cholesterol Metabolism Modulate Atherosclerosis in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2021Article
- Advances in Cardiovascular Biomarker Discovery.Biomedicines · 2020Review
- High-Density Lipoprotein (HDL) Inhibits Serum Amyloid A (SAA)-Induced Vascular and Renal Dysfunctions in Apolipoprotein E-Deficient Mice.International journal of molecular sciences · 2020Article
- Association between a urinary biomarker for exposure to PAH and blood level of the acute phase protein serum amyloid A in coke oven workers.Environmental health : a global access science source · 2019Article
- Role of serum amyloid A in atherosclerosis.Current opinion in lipidology · 2019Review
- Apoproteins E, A-I, and SAA in Macrophage Pathobiology Related to Atherogenesis.Frontiers in pharmacology · 2019Review
- Olive Leaf Extract Attenuates Inflammatory Activation and DNA Damage in Human Arterial Endothelial Cells.Frontiers in cardiovascular medicine · 2019Article
- Serum Amyloid A Stimulates Vascular and Renal Dysfunction in Apolipoprotein E-Deficient Mice Fed a Normal Chow Diet.Frontiers in immunology · 2019Article
- Serum amyloid A3 is a high density lipoprotein-associated acute-phase protein.Journal of lipid research · 2018Article
- Inflammation, remodeling, and other factors affecting HDL cholesterol efflux.Current opinion in lipidology · 2017Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundAtherosclerosis is a chronic inflammatory disorder, and several studies have demonstrated a positive association between plasma serum amyloid A (SAA) levels and cardiovascular disease risk. The aim of the study was to examine whether SAA has a role in atherogenesis, the underlying basis of most cardiovascular disease. METHODS AND
resultsMice globally deficient in acute-phase isoforms Saa1 and Saa2 (Saa(-/-)) were crossed to Ldlr(-/-) mice (Saa(-/-)Ldlr(-/-)). Saa(-/-)Ldlr(-/-) mice demonstrated a 31% reduction in lesional area in the ascending aorta but not in the aortic root or innominate artery after consuming a high-fat, high-cholesterol Western-type diet for 6 weeks. The lesions were predominantly macrophage foam cells. The phenotype was lost in more mature lesions in mice fed a Western-type diet for 12 weeks, suggesting that SAA is involved in early lesion development. The decreased atherosclerosis in the Saa(-/-)Ldlr(-/-) mice occurred despite increased levels of blood monocytes and was independent of plasma lipid levels. SAA is produced predominantly by hepatocytes and macrophages. To determine which source of SAA may have a dominant role in lesion development, bone marrow transplantation was performed. Ldlr(-/-) mice that received bone marrow from Saa(-/-)Ldlr(-/-) mice had slightly reduced ascending aorta atherosclerosis compared with Saa(-/-)Ldlr(-/-) mice receiving bone marrow from Ldlr(-/-) mice, indicating that the expression of SAA by macrophages may have an important influence on atherogenesis.
conclusionsThe results indicate that SAA produced by macrophages promotes early lesion formation in the ascending aorta.
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