{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,6]],"date-time":"2025-11-06T17:59:12Z","timestamp":1762451952435,"version":"build-2065373602"},"reference-count":209,"publisher":"MDPI AG","issue":"21","license":[{"start":{"date-parts":[[2025,11,6]],"date-time":"2025-11-06T00:00:00Z","timestamp":1762387200000},"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>Heart failure with preserved ejection fraction (HFpEF) currently accounts for half of the heart failure (HF) cases world-wide, affecting nearly 32 million people. HFpEF has a skewed prevalence toward females and those older than 65 years old. The pathophysiology of HFpEF is suggestive of a conglomerate of inflammatory, hypertensive, as well as metabolic dysfunction, giving rise to the syndrome. Disruptions in ceramide metabolism do occur in heart failure as well as within the HFpEF-associated risk factors, both modifiable inflammation, obesity, hypertension, diabetes, and non-modifiable-aging, and female sex. The focus of this review is to draw attention to the links between changes in female biophysiology, such as pregnancy, menopause and aging, in which ceramide is dysregulated and consequently gives rise to the same pathologies that are labeled as risk factors for HFpEF. Our objective is to highlight ceramides as potential biomarkers for prevention and initial diagnostic tools for HFpEF, especially for women later in life.<\/jats:p>","DOI":"10.3390\/ijms262110800","type":"journal-article","created":{"date-parts":[[2025,11,6]],"date-time":"2025-11-06T17:51:43Z","timestamp":1762451503000},"page":"10800","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Ceramide as a Biomarker for HFpEF in Women: Menopause, Aging, and Pregnancy"],"prefix":"10.3390","volume":"26","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8296-8466","authenticated-orcid":false,"given":"Ruth R.","family":"Magaye","sequence":"first","affiliation":[{"name":"Heart Failure Research Group, Baker Heart and Diabetes Institute, Melbourne, VIC 3004, Australia"},{"name":"Monash Alfred Baker Centre for Cardiovascular Research, Monash University, Clayton, VIC 3800, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David M.","family":"Kaye","sequence":"additional","affiliation":[{"name":"Heart Failure Research Group, Baker Heart and Diabetes Institute, Melbourne, VIC 3004, Australia"},{"name":"Monash Alfred Baker Centre for Cardiovascular Research, Monash University, Clayton, VIC 3800, Australia"},{"name":"Department of Cardiology, Alfred Hospital, Melbourne, VIC 3004, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9580-2548","authenticated-orcid":false,"given":"Bing H.","family":"Wang","sequence":"additional","affiliation":[{"name":"Heart Failure Research Group, Baker Heart and Diabetes Institute, Melbourne, VIC 3004, Australia"},{"name":"Monash Alfred Baker Centre for Cardiovascular Research, Monash University, Clayton, VIC 3800, Australia"},{"name":"Biomarker Discovery Laboratory, Baker Heart and Diabetes Institute, Melbourne, VIC 3004, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1968","published-online":{"date-parts":[[2025,11,6]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"2265","DOI":"10.1042\/CS20210127","article-title":"Lipotoxicity: A driver of heart failure with preserved ejection fraction?","volume":"135","author":"Leggat","year":"2021","journal-title":"Clin. 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