{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,16]],"date-time":"2026-02-16T08:32:15Z","timestamp":1771230735833,"version":"3.50.1"},"reference-count":22,"publisher":"Wiley","issue":"14","license":[{"start":{"date-parts":[[2020,6,11]],"date-time":"2020-06-11T00:00:00Z","timestamp":1591833600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100004479","name":"Natural Science Foundation of Jiangxi Province","doi-asserted-by":"publisher","award":["20181BAB205003"],"award-info":[{"award-number":["20181BAB205003"]}],"id":[{"id":"10.13039\/501100004479","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100004479","name":"Natural Science Foundation of Jiangxi Province","doi-asserted-by":"publisher","award":["20192ACB21030"],"award-info":[{"award-number":["20192ACB21030"]}],"id":[{"id":"10.13039\/501100004479","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2020,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Increased expression and activity of cardiac and circulating cathepsin D and soluble fms\u2010like tyrosine kinase\u20101 (sFlt\u20101) have been demonstrated to induce and promote peripartum cardiomyopathy (PPCM) via promoting cleavage of 23\u2010kD prolactin (PRL) to 16\u2010kD PRL and neutralizing vascular endothelial growth factor (VEGF), respectively. We hypothesized that activation of Hes1 is proposed to suppress cathepsin D via activating Stat3, leading to alleviated development of PPCM. In the present study, we aimed to investigate the role of Notch1\/Hes1 pathway in PPCM. Pregnant mice between prenatal 3\u00a0days and postpartum 3\u00a0weeks were fed with LY\u2010411575 (a notch inhibitor, 10\u00a0mg\/kg\/d). Ventricular function and pathology were evaluated by echocardiography and histological analysis. Western blotting analysis was used to examine the expression at the protein level. The results found that inhibition of Notch1 significantly promoted postpartum ventricular dilatation, myocardial hypertrophy and myocardial interstitial fibrosis and suppressed myocardial angiogenesis. Western blotting analysis showed that inhibition of Notch1 markedly increased cathepsin D and sFlt\u20101, reduced Hes1, phosphorylated Stat3 (p\u2010Stat3), VEGFA and PDGFB, and promoted cleavage of 23k\u2010D PRL to 16\u2010kD PRL. Collectively, inhibition of Notch1\/Hes1 pathway induced and promoted PPCM via increasing the expressions of cathepsin D and sFlt\u20101. Notch1\/Hes1 was a promising target for prevention and therapeutic regimen of PPCM.<\/jats:p>","DOI":"10.1111\/jcmm.15423","type":"journal-article","created":{"date-parts":[[2020,6,12]],"date-time":"2020-06-12T00:58:53Z","timestamp":1591923533000},"page":"7907-7914","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["Inhibition of the Notch1 pathway induces peripartum cardiomyopathy"],"prefix":"10.1111","volume":"24","author":[{"given":"Rong\u2010rong","family":"Zhu","sequence":"first","affiliation":[{"name":"Department of Obstetrics and Gynecology High\u2010Tech Hospital The First Affiliated Hospital Nanchang University Nanchang China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Qian","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Cardiology the Second Medical Center, Chinese PLA General Hospital, National Clinical Research Center for Geriatric Diseases Beijing 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