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Among its heterogeneous subtypes, cardiometabolic HFpEF, which is driven by metabolic dysfunction, represents a globally predominant form. Recent advances in preclinical models have highlighted metabolic disturbances and systemic inflammation as key contributors to HFpEF pathogenesis. While much attention has focused on classical inflammatory mediators such as interleukin-6 (IL-6) and tumor necrosis factor-\u03b1 (TNF-\u03b1), the full spectrum of upstream inflammatory drivers and the therapeutic strategies targeting inflammation in cardiometabolic HFpEF remain incompletely defined. Among emerging candidates, serum amyloid A (SAA) family proteins, highly inducible acute-phase proteins, have attracted growing attention due to their elevated levels in chronic metabolic diseases. Here, we summarize clinical associations between elevated SAA levels and major cardiometabolic conditions\u2014including obesity, diabetes, metabolic dysfunction-associated steatotic liver disease (MASLD, formerly NAFLD), and hypertension\u2014and discuss potential mechanisms based on preclinical studies. We place particular emphasis on the known and potential pathogenetic role of SAA in cardiometabolic HFpEF, where it may contribute to systemic inflammation, endothelial dysfunction, and myocardial fibrosis. Overall, this review aims to advance understanding of SAA in HFpEF and cardiometabolic disease, and to support translational efforts toward improved diagnosis and treatment.<\/jats:p>","DOI":"10.1007\/s00395-025-01150-9","type":"journal-article","created":{"date-parts":[[2025,11,28]],"date-time":"2025-11-28T08:55:26Z","timestamp":1764320126000},"page":"1-21","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Serum amyloid A in HFpEF and cardiometabolic diseases"],"prefix":"10.1007","volume":"121","author":[{"given":"Luo","family":"Liu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rongling","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stefano","family":"Strocchi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tolga","family":"Eroglu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Natasha","family":"Nambiar","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarah V.","family":"Li\u00e9vano Contreras","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Saskia A.","family":"Diezel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7582-7171","authenticated-orcid":false,"given":"Gabriele G.","family":"Schiattarella","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,11,28]]},"reference":[{"key":"1150_CR1","doi-asserted-by":"publisher","first-page":"1119227","DOI":"10.3389\/fendo.2023.1119227","volume":"14","author":"S Abouelasrar Salama","year":"2023","unstructured":"Abouelasrar Salama S, Gouwy M, Van Damme J, Struyf S (2023) Acute-serum amyloid A and A-SAA-derived peptides as formyl peptide receptor (FPR) 2 ligands. 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