{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,10]],"date-time":"2026-02-10T16:53:04Z","timestamp":1770742384276,"version":"3.49.0"},"reference-count":47,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2022,12,13]],"date-time":"2022-12-13T00:00:00Z","timestamp":1670889600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81530012"],"award-info":[{"award-number":["81530012"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Phytotherapy Research"],"published-print":{"date-parts":[[2023,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Salidroside, a prominent active ingredient in traditional Chinese medicines, is garnering increased attention because of its unique pharmacological effects against ischemic heart disease via MAPK signaling, which plays a critical role in regulating the evolution of ventricular hypertrophy. However, the function of Salidroside on myocardial hypertrophy has not yet been elucidated. C57BL\/6 mice were subjected to transverse aortic constriction (TAC), and treated with Salidroside (100\u2009mg\u2009kg<jats:sup>\u22121<\/jats:sup>\u00a0day<jats:sup>\u22121<\/jats:sup>) by oral gavage for 3\u2009weeks starting 1\u2009week after surgery. Four weeks after TAC surgery, the mice were subjected to echocardiography and then sacrificed to harvest the hearts for analysis. For in vitro study, neonatal rat cardiomyocytes were used to validate the protective effects of Salidroside in response to Angiotensin II (Ang II, 1\u00a0\u03bcM) stimulation. Here, we proved that Salidroside dramatically inhibited hypertrophic reactions generated by pressure overload and isoproterenol (ISO) injection. Salidroside prevented the activation of the TAK1\u2010JNK\/p38 axis. Salidroside pretreatment of TAK1\u2010inhibited cardiomyocytes shows no additional attenuation of Ang II\u2010induced cardiomyocytes hypertrophy and signaling pathway activation. The overexpression of constitutively active TAK1 removed the protective effects of Salidroside on myocardial hypertrophy. TAC\u2010induced increase of TLR4 protein expression was reduced considerably in the Salidroside treated mice. Transient transfection of small interfering RNA targeting TLR4 (siTLR4) in cardiomyocytes did not further decrease the activation of the TAK1\/JNK\u2010p38 axis. In conclusion, Salidroside functioned as a TLR4 inhibitor and displayed anti\u2010hypertrophic action via the TAK1\/JNK\u2010p38 pathway.<\/jats:p>","DOI":"10.1002\/ptr.7701","type":"journal-article","created":{"date-parts":[[2022,12,13]],"date-time":"2022-12-13T16:22:24Z","timestamp":1670948544000},"page":"1839-1849","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Salidroside ameliorates pathological cardiac hypertrophy via <scp>TLR4\u2010TAK1<\/scp>\u2010dependent signaling"],"prefix":"10.1002","volume":"37","author":[{"given":"Zhen","family":"Guo","sequence":"first","affiliation":[{"name":"Department of Cardiology Renmin Hospital of Wuhan University  Wuhan People's Republic of China"},{"name":"Hubei Key Laboratory of Metabolic and Chronic Diseases  Wuhan People's Republic of 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