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In our research, <jats:italic>Tmem173<\/jats:italic> global knockout (KO) mice manifested more deteriorated hypertrophy, fibrosis, inflammatory infiltration and cardiac malfunction compared with wild type C57BL\/6 mice after 6 weeks of transverse aortic constriction. And KO mice showed inhibited autophagosome degradation in myocardium observed under transmission electron microscope and in protein level. In in vitro experiments conducted in neonatal rat cardiomyocytes under phenylephrine treatment, the abundance of <jats:italic>Tmem173<\/jats:italic> gene was negatively related to the abundance of LC3\u2010\u2161 and the number of red and yellow fluorescent dots, of which reflected the capacity of autophagosome degradation. These results indicated that TMEM173 might be a promoter of autophagic flux and protected against pressure overload\u2010induced cardiac hypertrophy. It may serve as a potential therapeutic target for cardiac hypertrophy in the future.<\/jats:p>","DOI":"10.1002\/jcp.30223","type":"journal-article","created":{"date-parts":[[2020,12,25]],"date-time":"2020-12-25T02:30:20Z","timestamp":1608863420000},"page":"5176-5192","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["TMEM173 protects against pressure overload\u2010induced cardiac hypertrophy by modulating autophagy"],"prefix":"10.1002","volume":"236","author":[{"given":"Ya\u2010Ge","family":"Jin","sequence":"first","affiliation":[{"name":"Department of Cardiology, Renmin Hospital of Wuhan University Cardiovascular Research Institute of Wuhan University  Wuhan China"},{"name":"Hubei Key Laboratory of Metabolic and Chronic Diseases  Wuhan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Heng","family":"Zhou","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Renmin Hospital 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