{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["2025"],"submitter":["Sheng S"],"pubmed_abstract":["<b>Background:</b> Yes-associated protein (YAP) is a major downstream nuclear coactivator of the Hippo pathway and is activated during myocardial hypertrophy. Verteporfin, a YAP inhibitor, may serve as a potential treatment for myocardial hypertrophy. <b>Aim:</b> This study was aimed at exploring the role and underlying mechanisms of verteporfin in isoproterenol (ISO)-induced myocardial hypertrophy both in vivo and in vitro. <b>Methods:</b> GSE18801 directs our focus toward the Hippo pathway role in myocardial hypertrophy. Using an ISO-induced myocardial hypertrophy rat model, YAP expression and localization were observed through Western blot and immunofluorescence. Histopathological analysis was performed to evaluate cardiomyocyte cross-sectional area, and echocardiographic examinations were conducted to assess cardiac function. In vitro, primary neonatal rat cardiomyocytes (NRCMs) were cultured with conditioned medium from cardiac fibroblasts (CF-CM) treated with ISO to observe cell hypertrophy. Mechanistically, GSE203358 dataset analysis, enzyme-linked immunosorbent assay (ELISA), and Western blot were utilized to investigate the effects of ISO and verteporfin on IL-6, STAT3, and p-STAT3 levels in CFs. Subsequently, the changes in the IL-6/STAT3 pathway were evaluated in CFs treated with ISO and verteporfin. Additionally, recombinant IL-6 and IL-6 inhibitor were applied to CMs treated with CF-CM to observe changes in cardiomyocyte size. <b>Results:</b> Verteporfin improved cardiac performance in rats receiving ISO. In cultured NRCM, both ISO and CF-CM treated with ISO could induce cardiomyocyte hypertrophy. Verteporfin did not attenuate ISO-induced cardiomyocyte hypertrophy. However, it could attenuate hypertrophy induced by the CF-CM treated with ISO. GSE203358 indicated the involvement of the IL-6/STAT3 pathway in the presence of verteporfin in CFs. Additionally, verteporfin reduces IL-6 production in cultured CFs subjected to ISO treatment. Notably, the effects of verteporfin on NRCM were reversed by IL-6. <b>Conclusions:</b> Verteporfin protects the heart against ISO-induced myocardial hypertrophy by regulating IL-6/STAT3 in cardiac fibroblasts."],"journal":["Cardiovascular therapeutics"],"pagination":["2852780"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12411024"],"repository":["biostudies-literature"],"pubmed_title":["Verteporfin Mitigates Isoproterenol-Induced Myocardial Hypertrophy by Attenuating IL-6/STAT3 in Cardiac Fibroblasts."],"pmcid":["PMC12411024"],"pubmed_authors":["Lai J","Zhao R","Fan J","Ma J","Jin P","Sheng S","Chen S","Ding L","Ye Z"],"additional_accession":[]},"is_claimable":false,"name":"Verteporfin Mitigates Isoproterenol-Induced Myocardial Hypertrophy by Attenuating IL-6/STAT3 in Cardiac Fibroblasts.","description":"<b>Background:</b> Yes-associated protein (YAP) is a major downstream nuclear coactivator of the Hippo pathway and is activated during myocardial hypertrophy. Verteporfin, a YAP inhibitor, may serve as a potential treatment for myocardial hypertrophy. <b>Aim:</b> This study was aimed at exploring the role and underlying mechanisms of verteporfin in isoproterenol (ISO)-induced myocardial hypertrophy both in vivo and in vitro. <b>Methods:</b> GSE18801 directs our focus toward the Hippo pathway role in myocardial hypertrophy. Using an ISO-induced myocardial hypertrophy rat model, YAP expression and localization were observed through Western blot and immunofluorescence. Histopathological analysis was performed to evaluate cardiomyocyte cross-sectional area, and echocardiographic examinations were conducted to assess cardiac function. In vitro, primary neonatal rat cardiomyocytes (NRCMs) were cultured with conditioned medium from cardiac fibroblasts (CF-CM) treated with ISO to observe cell hypertrophy. Mechanistically, GSE203358 dataset analysis, enzyme-linked immunosorbent assay (ELISA), and Western blot were utilized to investigate the effects of ISO and verteporfin on IL-6, STAT3, and p-STAT3 levels in CFs. Subsequently, the changes in the IL-6/STAT3 pathway were evaluated in CFs treated with ISO and verteporfin. Additionally, recombinant IL-6 and IL-6 inhibitor were applied to CMs treated with CF-CM to observe changes in cardiomyocyte size. <b>Results:</b> Verteporfin improved cardiac performance in rats receiving ISO. In cultured NRCM, both ISO and CF-CM treated with ISO could induce cardiomyocyte hypertrophy. Verteporfin did not attenuate ISO-induced cardiomyocyte hypertrophy. However, it could attenuate hypertrophy induced by the CF-CM treated with ISO. GSE203358 indicated the involvement of the IL-6/STAT3 pathway in the presence of verteporfin in CFs. Additionally, verteporfin reduces IL-6 production in cultured CFs subjected to ISO treatment. Notably, the effects of verteporfin on NRCM were reversed by IL-6. <b>Conclusions:</b> Verteporfin protects the heart against ISO-induced myocardial hypertrophy by regulating IL-6/STAT3 in cardiac fibroblasts.","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025","modification":"2026-05-29T03:08:03.037Z","creation":"2026-05-29T03:05:35.041Z"},"accession":"S-EPMC12411024","cross_references":{"pubmed":["40919415"],"doi":["10.1155/cdr/2852780"]}}