{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,10]],"date-time":"2026-09-10T17:43:57Z","timestamp":1789062237920,"version":"build-2803163510"},"reference-count":22,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2020,2,19]],"date-time":"2020-02-19T00:00:00Z","timestamp":1582070400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2020,2,19]],"date-time":"2020-02-19T00:00:00Z","timestamp":1582070400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100011002","name":"National Natural Science Foundation of China-Yunnan Joint Fund","doi-asserted-by":"publisher","award":["81600280"],"award-info":[{"award-number":["81600280"]}],"id":[{"id":"10.13039\/501100011002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100011002","name":"National Natural Science Foundation of China-Yunnan Joint Fund","doi-asserted-by":"publisher","award":["81870290"],"award-info":[{"award-number":["81870290"]}],"id":[{"id":"10.13039\/501100011002","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":[[2020,4]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    To investigate the prevention of cardiac remodelling and inflammatory immune response after myocardial infarction (MI) via ACEI regulating dendritic cells (DCs), we explored whether the protective effect of ACEI was repressed under hyperlipidemic environment. In vivo, the survival rate and left ventricular function of the mice were recorded on day 7 after MI. Tissue samples of the myocardium, spleen, bone marrow and peripheral blood were assessed for Ang II concentration, inflammatory cytokines and DCs expression. In vitro, DCs were treated with ox\u2010LDL\u00a0+\u00a0Ang II, simulating the internal environment of MI in ApoE\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice to explore the mechanism involved in the DCs maturation and inflammation. Under hyperlipidemic circumstances, we found that the cardioprotective effect of ACEI was attenuated through regulating DCs maturation and inflammation after MI, affecting survival rate and left ventricular function. Effects of lisinopril on the release of spleen\u2010derived DCs and myocardial infiltration were also reduced under hyperlipidemic conditions. In vitro, immune maturation and inflammation of DCs were further induced by ox\u2010LDL on the basis of Ang II treatment, as indicated by the upregulation of CD83, CD86, and the expressions of cytokines and chemokines. Furthermore, ox\u2010LDL could activate TLR4\u2010MyD88 signalling pathway, promoting IRAK\u20104 and NF\u2010\u03baB. The present study demonstrated that ACEI reduced the recruitment of DCs to the infarct site, leading to a higher survival rate and improved function. However, this effect was inhibited under hyperlipidemic environment. TLR4\u2010MyD88 signalling pathway may be responsible for the molecular mechanism involved in the immune maturation and inflammation of DCs induced by ox\u2010LDL.\n                  <\/jats:p>","DOI":"10.1111\/jcmm.15060","type":"journal-article","created":{"date-parts":[[2020,2,19]],"date-time":"2020-02-19T09:16:09Z","timestamp":1582103769000},"page":"4082-4091","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Hyperlipidemia inhibits the protective effect of lisinopril after myocardial infarction via activation of dendritic cells"],"prefix":"10.1111","volume":"24","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8588-8285","authenticated-orcid":false,"given":"Yuanji","family":"Ma","sequence":"first","affiliation":[{"name":"Department of Cardiology Zhongshan Hospital Fudan University Shanghai China"},{"name":"Shanghai Institute of Cardiovascular Diseases Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Leilei","family":"Ma","sequence":"additional","affiliation":[{"name":"Department of Cardiology Zhongshan Hospital Fudan University Shanghai China"},{"name":"Shanghai Institute of Cardiovascular Diseases Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiaqi","family":"Ma","sequence":"additional","affiliation":[{"name":"Department of Cardiology Zhongshan Hospital Fudan University Shanghai China"},{"name":"Shanghai Institute of Cardiovascular Diseases Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Runda","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Cardiology Zhongshan Hospital Fudan University Shanghai China"},{"name":"Shanghai Institute of Cardiovascular Diseases Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yunzeng","family":"Zou","sequence":"additional","affiliation":[{"name":"Department of Cardiology Zhongshan Hospital Fudan University Shanghai China"},{"name":"Shanghai Institute of Cardiovascular Diseases Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Junbo","family":"Ge","sequence":"additional","affiliation":[{"name":"Department of Cardiology Zhongshan Hospital Fudan University Shanghai China"},{"name":"Shanghai Institute of Cardiovascular Diseases Shanghai 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