{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,4]],"date-time":"2026-09-04T17:50:31Z","timestamp":1788544231710,"version":"build-2803163510"},"reference-count":34,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"18","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2018,9,18]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">Cardiac hypertrophy has been recognized as an important independent risk factor for the development of heart failure and increases the risk of cardiac morbidity and mortality. A disintegrin and metalloprotease 23 (ADAM23), a member of ADAM family, is involved in cancer and neuronal differentiation. Although ADAM23 is expressed in the heart, the role of ADAM23 in the heart and in cardiac diseases remains unknown.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              We observed that ADAM23 expression is decreased in both failing human hearts and hypertrophic mice hearts. Cardiac\u2010specific conditional ADAM23\u2010knockout mice significantly exhibited exacerbated cardiac hypertrophy, fibrosis, and dysfunction, whereas transgenic mice overexpressing ADAM23 in the heart exhibited reduced cardiac hypertrophy in response to pressure overload. Consistent results were also observed in angiotensin\n              <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\n              \u2010induced neonatal rat cardiomyocyte hypertrophy. Mechanistically, ADAM23 exerts anti\u2010hypertrophic effects by specifically targeting the focal adhesion kinase\u2010protein kinase B (FAK\u2010AKT) signaling cascade. Focal adhesion kinase inactivation by inhibitor (\n              <jats:styled-content style=\"fixed-case\">PF<\/jats:styled-content>\n              \u2010562271) greatly reversed the detrimental effects in ADAM23\u2010knockout mice subjected to aortic banding.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusion<\/jats:title>\n            <jats:p xml:lang=\"en\">Altogether, we identified ADAM23 as a negative regulator of cardiac hypertrophy through inhibiting focal adhesion kinase\u2010protein kinase B signaling pathway, which could be a promising therapeutic target for this malady.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.118.008604","type":"journal-article","created":{"date-parts":[[2018,9,17]],"date-time":"2018-09-17T21:08:34Z","timestamp":1537218514000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":26,"title":["ADAM23 in Cardiomyocyte Inhibits Cardiac Hypertrophy by Targeting FAK\u2010AKT Signaling"],"prefix":"10.1161","volume":"7","author":[{"given":"Mei","family":"Xiang","sequence":"first","affiliation":[{"name":"Department of Cardiology The Central Hospital of Wuhan Tongji Medical College Huazhong University of Science and Technology Wuhan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hongbo","family":"Luo","sequence":"additional","affiliation":[{"name":"Department of Cardiology The Central Hospital of Wuhan Tongji Medical College Huazhong University of Science and Technology Wuhan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jia","family":"Wu","sequence":"additional","affiliation":[{"name":"Key Laboratory for Molecular Diagnosis of Hubei Province The Central Hospital of Wuhan Tongji Medical College Huazhong University of Science and Technology Wuhan 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