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Resection or transplantation of visceral adipose tissue (VAT) blunted or exacerbated HFpEF phenotypes, respectively, in mice. VAT from HFpEF mice displayed greater weight and secreted more small extracellular vesicles (sEVs) than those from chow-fed mice. Either systemic inhibition of sEV secretion or VAT-specific knockdown of Rab27b (an indispensable GTPase for sEV secretion) protected against HFpEF. Discovery-driven experiments identified miR-295-3p within sEVs as a possible mediator of the VAT-heart axis, which impaired cardiac autophagy by binding to Ulk1 mRNA. MiR-295-3p antagomir treatment mitigated HFpEF phenotypes. Additionally, neonatal mouse cardiomyocytes (NMCMs) manifested blunted autophagic flux after treatment with plasma sEVs from HFpEF mice. Notably, HFpEF patients displayed downregulated cardiac Ulk1 and autophagy compared with healthy individuals. Restoration of cardiac autophagy with rapamycin or ULK1 overexpression via AAV-9 attenuated the HFpEF phenotype in mice.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>The present work unveils a mechanism whereby obesity promotes HFpEF progression, emphasizing the role of VAT-heart crosstalk. Specifically, VAT-derived sEVs, miR-295-3p, and the resultant disruption of cardiac autophagy contribute significantly to the pathogenesis of HFpEF.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/cvr\/cvag030","type":"journal-article","created":{"date-parts":[[2026,2,4]],"date-time":"2026-02-04T12:43:40Z","timestamp":1770209020000},"page":"510-526","source":"Crossref","is-referenced-by-count":6,"title":["Small extracellular vesicle-mediated adipocyte-cardiomyocyte crosstalk exacerbates heart failure with preserved ejection fraction"],"prefix":"10.1093","volume":"122","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0134-0958","authenticated-orcid":false,"given":"Qi","family":"Pan","sequence":"first","affiliation":[{"name":"Department of Cardiology, State Key Laboratory of Cardiovascular Disease, National Center for Cardiovascular Diseases, Fuwai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College , Beijing 100037 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for Cardiovascular Metabolic Renal Research (MRC), Deutsches Herzzentrum der Charit\u00e9 (DHZC), Charit\u00e9 -Universit\u00e4tsmedizin Berlin , Berlin ,","place":["Germany"]},{"name":"Translational Approaches in Heart Failure and Cardiometabolic Disease, Max Delbr\u00fcck Center for Molecular Medicine in the Helmholtz Association (MDC) , Berlin ,","place":["Germany"]},{"name":"DZHK (German Centre for Cardiovascular Research) , Partner Site Berlin, Berlin ,","place":["Germany"]},{"name":"Friede Springer Cardiovascular Prevention Center at Charit\u00e9\u2014Universit\u00e4tsmedizin, Berlin ,","place":["Germany"]},{"name":"Experimental and Clinical Research Center (ECRC), A Cooperation of Charit\u00e9-Universit\u00e4tsmedizin Berlin and Max Delbruck Center for Molecular Medicine (MDC) , Berlin ,","place":["Germany"]},{"name":"Division of Cardiology, Department of Advanced Biomedical Sciences, Federico II University , Naples 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