{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,18]],"date-time":"2026-10-18T02:32:04Z","timestamp":1792290724026,"version":"4.4.0"},"reference-count":37,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2025,5,5]],"date-time":"2025-05-05T00:00:00Z","timestamp":1746403200000},"content-version":"vor","delay-in-days":4,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Biochem &amp;amp; Molecular Tox"],"published-print":{"date-parts":[[2025,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:sec><jats:label\/><jats:p>Cardiovascular disease is a major health concern, with cardiac hypertrophy (CH) leading to heart failure and increased mortality. Although kallistatin has shown a protective effect against cardiovascular diseases, its role in CH remains unclear. The effects of kallistatin on myocardial lipid metabolism, inflammation, and hypertrophy via the SIRT1\/PPAR\u03b1 pathway in both animal model and cell culture were assessed. The rat model of CH was induced by Angiotensin II (Ang II). Plasma kallistatin and inflammatory indicators (IL\u20106, TNF\u2010\u03b1, MCP\u20101) were measured using ELISA. <jats:italic>In Vitro<\/jats:italic>, Ang II\u2010treated NRVMs were divided into control, Ang II, and Ang II + kallistatin groups. WGA\u2010Oregon Red staining was used to assess cell size, and CO\u2010IP was performed to evaluate SIRT1\/PPAR\u03b1 interactions. Gene (ANF, \u03b1\u2010SKA, PDK4, mCPT\u2010I, MCAD) and protein expression in NRVMs and heart tissues were analyzed via qRT\u2010PCR and Western blot. Kallistatin levels were decreased in patients with CH and rats with Ang II\u2010induced CH. <jats:italic>In Vivo<\/jats:italic>, kallistatin treatment decreased the HW\/BW ratio, SBP, DBP and MAP, cardiomyocyte size, and arrhythmias. <jats:italic>In Vitro<\/jats:italic>, kallistatin reversed Ang II\u2010induced hypertrophy, evidenced by smaller cell size (via WGA\u2010Oregon Red staining), reduced ANF and \u03b1\u2010SKA expression, and decreased lipid accumulation. Kallistatin inhibited inflammatory markers (IL\u20106, TNF\u2010\u03b1, MCP\u20101) and enhanced fatty acid oxidation by upregulating PDK4, mCPT\u2010I, and MCAD. CO\u2010IP demonstrated interactions between SIRT1 and PPAR\u03b1, and pathway inhibition confirmed that kallistatin's protective effects were mediated through the SIRT1\/PPAR\u03b1 pathway. Kallistatin protects against CH and arrhythmias reducing inflammation and improving lipid metabolism by modulating the SIRT1\/PPAR\u03b1 pathway.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jbt.70274","type":"journal-article","created":{"date-parts":[[2025,5,5]],"date-time":"2025-05-05T03:04:50Z","timestamp":1746414290000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Kallistatin Improves Lipid Metabolism and Alleviates Cardiac Hypertrophy via the SIRT1\/PPAR Pathway: An Experimental Study"],"prefix":"10.1002","volume":"39","author":[{"given":"Bing","family":"Li","sequence":"first","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, The Key Laboratory of Neural and Vascular Biology, China Administration of Education Hebei Medical University Shijiazhuang Hebei China"},{"name":"Department of Cardiology Cangzhou Central Hospital Cangzhou Hebei 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