{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T02:20:26Z","timestamp":1773454826932,"version":"3.50.1"},"reference-count":58,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2018,6,20]],"date-time":"2018-06-20T00:00:00Z","timestamp":1529452800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81573433"],"award-info":[{"award-number":["81573433"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2018,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:label\/><jats:p>Cardiac hypertrophy is one of the major risk factors for chronic heart failure. The role of endophilinA2 (EndoA2) in clathrin\u2010mediated endocytosis and clathrin\u2010independent endocytosis is well documented. In the present study, we tested the hypothesis that EndoA2 protects against angiotensin II (Ang II)\u2010induced cardiac hypertrophy by mediating intracellular angiotensin II type 1 receptor (AT1\u2010R) trafficking in neonatal rat cardiomyocytes (NRCMs). Cardiac hypertrophy was evaluated by using cell surface area and quantitative RT\u2010PCR (qPCR) analyses. For the first time, we found that EndoA2 attenuated cardiac hypertrophy and fibrosis induced by Ang II. Moreover, EndoA2 inhibited apoptosis induced by excessive endoplasmic reticulum stress (ERS), which accounted for the beneficial effects of EndoA2 on cardiac hypertrophy. We further revealed that there was an interaction between EndoA2 and AT1\u2010R.The expression levels of EndoA2, which inhibits AT1\u2010R transport from the cytoplasm to the membrane, and the interaction between EndoA2 and AT1\u2010R were obviously decreased after Ang II treatment. Furthermore, Ang II inhibited the co\u2010localization of AT1\u2010R with GRP\u201078, which was reversed by EndoA2 overexpression. In conclusion, our results suggested that EndoA2 plays a role in protecting against cardiac hypertrophy induced by Ang II, possibly by inhibiting AT1\u2010R transport from the cytoplasm to the membrane to suppress signal transduction.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jcb.26862","type":"journal-article","created":{"date-parts":[[2018,6,20]],"date-time":"2018-06-20T08:07:36Z","timestamp":1529482056000},"page":"8290-8303","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["EndophilinA2 protects against angiotensin II\u2010induced cardiac hypertrophy by inhibiting angiotensin II type 1 receptor trafficking in neonatal rat cardiomyocytes"],"prefix":"10.1002","volume":"119","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5813-9046","authenticated-orcid":false,"given":"Yun","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Pharmacology School of Pharmaceutical Sciences and the Fifth Affiliated Hospital Guangzhou Medical University Guangzhou P.R. 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