{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T17:00:08Z","timestamp":1791046808848,"version":"4.1.0"},"reference-count":98,"publisher":"MDPI AG","issue":"1","license":[{"start":{"date-parts":[[2025,12,25]],"date-time":"2025-12-25T00:00:00Z","timestamp":1766620800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Serum Amyloid A (SAA) is an acute-phase apolipoprotein that acts as both a sensitive biomarker of systemic inflammation and an active modulator of lipid metabolism and vascular homeostasis. This review summarises current insights into the interaction between SAA and high-density lipoproteins (HDL), with particular emphasis on its role in inflammation-driven cardiovascular disease (CVD). The incorporation of SAA into HDL markedly alters its composition and function. The displacement of apolipoprotein A-I impairs cholesterol efflux capacity, reduces antioxidative activity, and promotes a pro-inflammatory phenotype, transforming protective HDL into a dysfunctional particle. These changes contribute to endothelial dysfunction, foam cell formation, and atherogenesis. Elevated SAA levels are also associated with adverse cardiovascular and metabolic outcomes, including coronary artery disease, type 2 diabetes, and chronic kidney disease. Isoform-specific variations in SAA\u2013HDL interactions are emerging as key modulators of these effects. This review also discusses emerging therapeutic and nutritional strategies to modulate the SAA\u2013HDL axis, including anti-inflammatory therapies, HDL mimetics, and diet-based interventions. Future research should prioritise the standardisation of SAA measurement, characterisation of isoform-specific functions, and translational studies integrating SAA into cardiovascular risk stratification and therapy.<\/jats:p>","DOI":"10.3390\/ijms27010241","type":"journal-article","created":{"date-parts":[[2025,12,26]],"date-time":"2025-12-26T00:50:21Z","timestamp":1766710221000},"page":"241","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Serum Amyloid A (SAA) and Its Interaction with High-Density Lipoprotein Cholesterol (HDL-C): A Comprehensive Review"],"prefix":"10.3390","volume":"27","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0302-2136","authenticated-orcid":false,"given":"Angela P.","family":"Moissl-Blanke","sequence":"first","affiliation":[{"name":"Department of Medicine I (Cardiology, Angiology, Hemostaseology, Intensive Care), Medical Faculty Mannheim, University of Heidelberg, 68167 Mannheim, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Graciela E.","family":"Delgado","sequence":"additional","affiliation":[{"name":"LURIC Study GmbH, Josef-M\u00f6rtl-Stra\u00dfe 23, 86482 Aystetten, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1718-2918","authenticated-orcid":false,"given":"Bernhard K.","family":"Kr\u00e4mer","sequence":"additional","affiliation":[{"name":"Department of Medicine, Medical Faculty Mannheim, University of Heidelberg, 68167 Mannheim, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R\u00fcdiger","family":"Siekmeier","sequence":"additional","affiliation":[{"name":"Federal Institute for Drugs and Medical Services, 53175 Bonn, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5249-4012","authenticated-orcid":false,"given":"Daniel","family":"Duerschmied","sequence":"additional","affiliation":[{"name":"Department of Medicine I (Cardiology, Angiology, Hemostaseology, Intensive Care), Medical Faculty Mannheim, University of Heidelberg, 68167 Mannheim, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6083-8946","authenticated-orcid":false,"given":"Winfried","family":"M\u00e4rz","sequence":"additional","affiliation":[{"name":"LURIC Study GmbH, Josef-M\u00f6rtl-Stra\u00dfe 23, 86482 Aystetten, Germany"},{"name":"Department of Medicine III (Cardiology, Pneumonology, Angiology), Medical Faculty Heidelberg, University of Heidelberg, 69120 Heidelberg, Germany"},{"name":"SYNLAB Academy, SYNLAB Holding Deutschland GmbH, 68161 Mannheim, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0663-7275","authenticated-orcid":false,"given":"Marcus E.","family":"Kleber","sequence":"additional","affiliation":[{"name":"Department of Medicine I (Cardiology, Angiology, Hemostaseology, Intensive Care), Medical Faculty Mannheim, University of Heidelberg, 68167 Mannheim, Germany"},{"name":"LURIC Study GmbH, Josef-M\u00f6rtl-Stra\u00dfe 23, 86482 Aystetten, Germany"},{"name":"SYNLAB MVZ f\u00fcr Humangenetik Mannheim GmbH, 68163 Mannheim, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2025,12,25]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","unstructured":"Sori\u0107 Hosman, I., Kos, I., and Lamot, L. 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