{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,26]],"date-time":"2026-10-26T01:16:11Z","timestamp":1792977371894,"version":"4.5.0"},"reference-count":41,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"14","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2023,7,18]]},"abstract":"<jats:sec sec-type=\"background\" xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">Heart failure with preserved ejection fraction (HFpEF) is a significant unmet need in cardiovascular medicine and remains an untreatable cardiovascular disease. The role and mechanism of interleukin\u20101\u03b2 in HFpEF pathogenesis are poorly understood.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              C57\/Bl6J and interleukin\u20101\u03b2\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              male mice were randomly divided into 4 groups. Groups 1 and 2: C57\/Bl6J and interleukin\u20101\u03b2\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              mice were fed a regular diet for 4\u2009months and considered controls. Groups 3 and 4: C57\/Bl6 and interleukin\u20101\u03b2\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              mice were fed a high\u2010fat diet with N[w]\u2010nitro\u2010l\u2010arginine methyl ester (endothelial nitric oxide synthase inhibitor, 0.5\u2009g\/L) in the drinking water for 4\u2009months. We measured body weight, blood pressure, diabetes status, cardiac function\/hypertrophy\/inflammation, fibrosis, vascular endothelial function, and signaling. C57\/Bl6 fed a high\u2010fat diet and N[w]\u2010nitro\u2010l\u2010arginine methyl ester in the drinking water for 4\u2009months developed HFpEF pathogenesis characterized by obesity, diabetes, hypertension, cardiac hypertrophy, lung edema, low running performance, macrovascular and microvascular endothelial dysfunction, and diastolic cardiac dysfunction but no change in cardiac ejection fraction compared with control mice. Interestingly, the genetic disruption of interleukin\u20101\u03b2 protected mice from HFpEF pathogenesis through the modulation of the inflammation and endoplasmic reticulum stress mechanisms.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">Our data suggest that interleukin\u20101\u03b2 is a critical driver in the development of HFpEF pathogenesis, likely through regulating inflammation and endoplasmic reticulum stress pathways. Our findings provide a potential therapeutic target for HFpEF treatment.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.122.029668","type":"journal-article","created":{"date-parts":[[2023,6,22]],"date-time":"2023-06-22T21:30:50Z","timestamp":1687469450000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":18,"title":["Interleukin\u20101\u03b2 Disruption Protects Male Mice From Heart Failure With Preserved Ejection Fraction Pathogenesis"],"prefix":"10.1161","volume":"12","author":[{"given":"Balaji K.","family":"Srinivas","sequence":"first","affiliation":[{"name":"Department of Physiological Sciences EVMS Norfolk VA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aya","family":"Bourdi","sequence":"additional","affiliation":[{"name":"Department of Physiological Sciences EVMS Norfolk VA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jacob 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