{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,15]],"date-time":"2026-07-15T03:29:13Z","timestamp":1784086153873,"version":"3.55.0"},"reference-count":39,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2022,4,1]],"date-time":"2022-04-01T00:00:00Z","timestamp":1648771200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2022,4,1]],"date-time":"2022-04-01T00:00:00Z","timestamp":1648771200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2022,5]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Pathological cardiac hypertrophy is the most important risk factor for developing chronic heart failure. Therefore, the discovery of novel agents for treating pathological cardiac hypertrophy remains urgent. In the present study, we examined the therapeutic effect and mechanism of periplocymarin (PM)\u2010mediated protection against pathological cardiac hypertrophy using angiotensinII (AngII)\u2010stimulated cardiac hypertrophy in H9c2 cells and transverse aortic constriction (TAC)\u2010induced cardiac hypertrophy in mice. In vitro, PM treatment significantly reduced the surface area of H9c2 cells and expressions of hypertrophy\u2010related proteins. Meanwhile, PM markedly down\u2010regulated AngII\u2010induced translocation of\n                    <jats:italic>p<\/jats:italic>\n                    \u2010STAT3 into the nuclei and enhanced the phosphorylation levels of JAK2 and STAT3 proteins. The STAT3\u00a0specific inhibitor S3I\u2010201 or siRNA\u2010mediated depleted expression could alleviate AngII\u2010induced cardiac hypertrophy in H9c2 cells following PM treatment; however, PM failed to reduce the expressions of hypertrophy\u2010related proteins and phosphorylated STAT3 in STAT3\u2010overexpressing cells, indicating that PM protected against AngII\u2010induced cardiac hypertrophy by modulating STAT3\u00a0signalling. In vivo, PM reversed TAC\u2010induced cardiac hypertrophy, as determined by down\u2010regulating ratios of heart weight to body weight (HW\/BW), heart weight to tibial length (HW\/TL) and expressions of hypertrophy\u2010related proteins accompanied by the inhibition of the JAK2\/STAT3 pathway. These results revealed that PM could effectively protect the cardiac structure and function in experimental models of pathological cardiac hypertrophy by inhibiting the JAK2\/STAT3\u00a0signalling pathway. PM is expected to be a potential lead compound of the novel agents for treating pathological cardiac hypertrophy.\n                  <\/jats:p>","DOI":"10.1111\/jcmm.17267","type":"journal-article","created":{"date-parts":[[2022,4,2]],"date-time":"2022-04-02T02:43:03Z","timestamp":1648867383000},"page":"2607-2619","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["Periplocymarin alleviates pathological cardiac hypertrophy via inhibiting the JAK2\/STAT3 signalling pathway"],"prefix":"10.1111","volume":"26","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4213-8932","authenticated-orcid":false,"given":"Cai\u2010lian","family":"Fan","sequence":"first","affiliation":[{"name":"Department of Cardiology Jinan University First Affiliated Hospital Jinan University  Guangzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sui","family":"Liang","sequence":"additional","affiliation":[{"name":"Department 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