{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T04:16:51Z","timestamp":1791001011663,"version":"4.1.0"},"reference-count":38,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2016,1,14]],"date-time":"2016-01-14T00:00:00Z","timestamp":1452729600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Natural Science Funding of China","award":["21472142"],"award-info":[{"award-number":["21472142"]}]},{"name":"Natural Science Funding of China","award":["81200572"],"award-info":[{"award-number":["81200572"]}]},{"name":"High-level Innovative Talent Funding of Zhejiang Department of Health","award":["2010-017"],"award-info":[{"award-number":["2010-017"]}]},{"name":"Zhejiang Key Group in Scientific Innovation","award":["2010R50042"],"award-info":[{"award-number":["2010R50042"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2016,3]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Cardiac hypertrophy is an important risk factor for heart failure. Epidermal growth factor receptor (\n                    <jats:styled-content style=\"fixed-case\">EGFR<\/jats:styled-content>\n                    ) has been found to play a role in the pathogenesis of various cardiovascular diseases. The aim of this current study was to examine the role of\n                    <jats:styled-content style=\"fixed-case\">EGFR<\/jats:styled-content>\n                    in angiotensin II (Ang II)\u2010induced cardiac hypertrophy and identify the underlying molecular mechanisms. In this study, we observed that both Ang II and\n                    <jats:styled-content style=\"fixed-case\">EGF<\/jats:styled-content>\n                    could increase the phospohorylation of\n                    <jats:styled-content style=\"fixed-case\">EGFR<\/jats:styled-content>\n                    and protein kinase B (AKT)\/extracellular signal\u2010regulated kinase (ERK), and then induce cell hypertrophy in H9c2 cells. Both pharmacological inhibitors and genetic silencing significantly reduced Ang II\u2010induced\n                    <jats:styled-content style=\"fixed-case\">EGFR<\/jats:styled-content>\n                    signalling pathway activation, hypertrophic marker overexpression, and cell hypertrophy. In addition, our results showed that Ang II\u2010induced\n                    <jats:styled-content style=\"fixed-case\">EGFR<\/jats:styled-content>\n                    activation is mediated by c\u2010Src phosphorylation.\n                    <jats:italic>In vivo<\/jats:italic>\n                    , Ang II treatment significantly led to cardiac remodelling including cardiac hypertrophy, disorganization and fibrosis, accompanied by the activation of\n                    <jats:styled-content style=\"fixed-case\">EGFR<\/jats:styled-content>\n                    signalling pathway in the heart tissues, while all these molecular and pathological alterations were attenuated by the oral administration with\n                    <jats:styled-content style=\"fixed-case\">EGFR<\/jats:styled-content>\n                    inhibitors. In conclusion, the c\u2010Src\u2010dependent\n                    <jats:styled-content style=\"fixed-case\">EGFR<\/jats:styled-content>\n                    activation may play an important role in Ang II\u2010induced cardiac hypertrophy, and inhibition of\n                    <jats:styled-content style=\"fixed-case\">EGFR<\/jats:styled-content>\n                    by specific molecules may be an effective strategy for the treatment of Ang II\u2010associated cardiac diseases.\n                  <\/jats:p>","DOI":"10.1111\/jcmm.12763","type":"journal-article","created":{"date-parts":[[2016,1,14]],"date-time":"2016-01-14T07:26:20Z","timestamp":1452756380000},"page":"482-494","source":"Crossref","is-referenced-by-count":55,"title":["Novel\n                    <scp>EGFR<\/scp>\n                    inhibitors attenuate cardiac hypertrophy induced by angiotensin 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