{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T01:50:13Z","timestamp":1788313813944,"version":"build-2803163510"},"reference-count":36,"publisher":"SAGE Publications","license":[{"start":{"date-parts":[[2025,7,18]],"date-time":"2025-07-18T00:00:00Z","timestamp":1752796800000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"},{"start":{"date-parts":[[2025,7,18]],"date-time":"2025-07-18T00:00:00Z","timestamp":1752796800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"funder":[{"name":"Qiqihar Science and Technology Program Joint Guidance Project","award":["LHYD-202047"],"award-info":[{"award-number":["LHYD-202047"]}]}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Hum Exp Toxicol"],"published-print":{"date-parts":[[2025,9]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Robinin possesses certain antioxidative and anti-inflammatory properties. However, its mechanisms of action in cardiac hypertrophy (CH) and fibrosis remain inadequately explored.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>An in vitro model of CH was established using angiotensin II-treated rat H9c2 cardiomyocytes treated with escalating concentrations of Robinin. For the in vivo model, pulmonary heart disease-induced CH in rats was induced by chronic hypercapnia and TAC. Myocardial cell markers were evaluated through qRT-PCR, Western blotting, ELISA, cellular immunofluorescence, and HE staining. The role of SIRT1 in Robinin\u2019s effects was determined using pharmacological inhibition with SIRT1-IN-1.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>In vitro, Robinin suppressed hypertrophic (ANP, BNP, \u03b2-MHC) and fibrotic markers (MyHC, Collagen I, TGF-\u03b21) and reduced NLRP3 components (IL-1\u03b2, IL-18, ASC, Caspase-1) and oxidative stress (OS, \u2193MDA, \u2191SOD\/HO-1\/Nrf2) in a dose-dependent manner. These effects were mediated by SIRT1 upregulation and NF-\u03baB inactivation. Crucially, SIRT1 inhibition abolished Robinin\u2019s protection against hypertrophy and inflammation. In vivo, Robinin attenuated pulmonary heart disease-induced hypertrophy, fibrosis, NLRP3 activation, and OS while restoring SIRT1\/NF-\u03baB balance.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Robinin alleviates CH in pulmonary heart disease by modulating the SIRT1\/NF-\u03baB pathway to suppress OS and NLRP3 inflammasome activation, establishing its novel therapeutic potential.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/09603271251361892","type":"journal-article","created":{"date-parts":[[2025,7,18]],"date-time":"2025-07-18T11:14:18Z","timestamp":1752837258000},"update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":4,"title":["Robinin attenuates cardiac hypertrophy in pulmonary heart disease by modulating SIRT1\/NF-\u03baB signaling and inhibiting oxidative stress and the NLRP3 inflammasome"],"prefix":"10.1177","volume":"44","author":[{"ORCID":"https:\/\/orcid.org\/0009-0006-8124-7129","authenticated-orcid":false,"given":"Chao","family":"Wang","sequence":"first","affiliation":[{"name":"The Second Affiliated Hospital of Qiqihar Medical University"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0005-3055-2142","authenticated-orcid":false,"given":"Lei","family":"Qin","sequence":"additional","affiliation":[{"name":"Qiqihar Medical University"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0009-3578-7484","authenticated-orcid":false,"given":"Xinrui","family":"Zhang","sequence":"additional","affiliation":[{"name":"The Second Affiliated Hospital of Qiqihar Medical University"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0005-4311-1231","authenticated-orcid":false,"given":"Yubao","family":"Liu","sequence":"additional","affiliation":[{"name":"The Second Affiliated Hospital of Qiqihar Medical University"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2025,7,18]]},"reference":[{"issue":"1","key":"e_1_3_5_2_2","first-page":"55","article-title":"Pulmonary hypertension in adults with congenital heart disease","volume":"40","author":"Goldstein SA","year":"2022","unstructured":"Goldstein SA, Krasuski RA. Pulmonary hypertension in adults with congenital heart disease. Cardiol Clin 2022; 40(1): 55\u201367.","journal-title":"Cardiol Clin"},{"key":"e_1_3_5_3_2","doi-asserted-by":"publisher","unstructured":"Wissm\u00fcller M Dohr J Adler J et al. Pulmonary hypertension associated with left heart disease. Herz. 2023 48(4): 266\u2013273. English. DOI: 10.1007\/s00059-023-05189-z.","DOI":"10.1007\/s00059-023-05189-z"},{"issue":"1","key":"e_1_3_5_4_2","first-page":"69","article-title":"Left heart disease-related pulmonary hypertension","volume":"40","author":"Alamri AK","year":"2022","unstructured":"Alamri AK, Ma CL, Ryan JJ. Left heart disease-related pulmonary hypertension. 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