{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T08:44:36Z","timestamp":1790671476073,"version":"4.1.0"},"reference-count":44,"publisher":"Wiley","issue":"18","license":[{"start":{"date-parts":[[2020,8,14]],"date-time":"2020-08-14T00:00:00Z","timestamp":1597363200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100002822","name":"Central South University","doi-asserted-by":"publisher","award":["JY201714"],"award-info":[{"award-number":["JY201714"]}],"id":[{"id":"10.13039\/501100002822","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":[[2020,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Ubiquitin\u2010specific protease 19 (USP19) belongs to USP family and is involved in promoting skeletal muscle atrophy. Although USP19 is expressed in the heart, the role of USP19 in the heart disease remains unknown. The present study provides in vivo and in vitro data to reveal the role of USP19 in preventing pathological cardiac hypertrophy. We generated USP19\u2010knockout mice and isolated neonatal rat cardiomyocytes (NRCMs) that overexpressed or were deficient in USP19 to investigate the effect of USP19 on transverse aortic constriction (TAC) or phenylephrine (PE)\u2010mediated cardiac hypertrophy. Echocardiography, pathological and molecular analysis were used to determine the extent of cardiac hypertrophy, fibrosis, dysfunction and inflammation. USP19 expression was markedly increased in rodent hypertrophic heart or cardiomyocytes underwent TAC or PE culturing, the increase was mediated by the reduction of Seven In Absentia Homolog\u20102. The extent of TAC\u2010induced cardiac hypertrophy, fibrosis, dysfunction and inflammation in USP19\u2010knockout mice was exacerbated. Consistently, gain\u2010of\u2010function and loss\u2010of\u2010function approaches that involved USP19 in cardiomyocytes suggested that the down\u2010regulation of USP19 promoted the hypertrophic phenotype, while the up\u2010regulation of USP19 improved the worsened phenotype. Mechanistically, the USP19\u2010elicited cardiac hypertrophy improvement was attributed to the abrogation of the transforming growth factor beta\u2010activated kinase 1 (TAK1)\u2010p38\/JNK1\/2 transduction. Furthermore, the inhibition of TAK1 abolished the aggravated hypertrophy induced by the loss of USP19. In conclusion, the present study revealed that USP19 and the downstream of TAK1\u2010p38\/JNK1\/2 signalling pathway might be a potential target to attenuate pathological cardiac hypertrophy.<\/jats:p>","DOI":"10.1111\/jcmm.15724","type":"journal-article","created":{"date-parts":[[2020,8,15]],"date-time":"2020-08-15T07:46:58Z","timestamp":1597477618000},"page":"10946-10957","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["Ubiquitin\u2010specific protease 19 blunts pathological cardiac hypertrophy via inhibition of the TAK1\u2010dependent pathway"],"prefix":"10.1111","volume":"24","author":[{"given":"Rujia","family":"Miao","sequence":"first","affiliation":[{"name":"Health Management Center The Third Xiangya Hospital Central South University Changsha China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yao","family":"Lu","sequence":"additional","affiliation":[{"name":"Department of Clinical 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