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The high prevalence of comorbidities such as diabetes, visceral obesity, and aging, which contribute to systemic inflammation, plays a pivotal role in the pathogenesis and progression of HFpEF. Glucagon-Like Peptide-1 Receptor Agonists (GLP-1 RAs), a class of glucose-lowering drugs, have demonstrated a wide range of pleiotropic effects that extend beyond glycaemic control. These effects include the reduction of inflammation and oxidative stress, vasodilation, decreased arterial stiffness, and a reduction in myocardial fibrosis\u2014key factors in the pathophysiology of HFpEF. Recent evidence from the STEP-HFpEF and STEP-HFpEF-DM trials provides the first robust data supporting the efficacy of GLP-1 RAs, specifically semaglutide, in improving the quality of life in obese patients with HFpEF. These trials also demonstrated a significant reduction in C-Reactive Protein (CRP) levels, reinforcing the hypothesis that suppressing the pro-inflammatory state may yield substantial clinical benefits in this patient population. These findings suggest that GLP-1 RAs could play a crucial role in the management of HFpEF, particularly in patients with obesity, by targeting the underlying inflammatory processes and contributing to better overall cardiovascular outcomes.<\/jats:p>","DOI":"10.1007\/s10741-024-10450-6","type":"journal-article","created":{"date-parts":[[2024,10,19]],"date-time":"2024-10-19T01:02:49Z","timestamp":1729299769000},"page":"131-136","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":58,"title":["GLP-1 receptor agonists as promising anti-inflammatory agents in heart failure with preserved ejection fraction"],"prefix":"10.1007","volume":"30","author":[{"given":"Giovanni Battista","family":"Bonfioli","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luca","family":"Rodella","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marco","family":"Metra","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3544-6104","authenticated-orcid":false,"given":"Enrico","family":"Vizzardi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2024,10,19]]},"reference":[{"issue":"21 Suppl 1","key":"10450_CR1","doi-asserted-by":"publisher","first-page":"II2","DOI":"10.1161\/01.CIR.0000129535.04194.38","volume":"109","author":"JT Willerson","year":"2004","unstructured":"Willerson JT, Ridker PM (2004) Inflammation as a cardiovascular risk factor. 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