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Nevertheless, current understanding of the influence of <jats:styled-content style=\"fixed-case\">TES<\/jats:styled-content> on cardiovascular diseases, especially on cardiac hypertrophy and its etiology, is insufficient. This study investigated the influence of <jats:styled-content style=\"fixed-case\">TES<\/jats:styled-content> on cardiac hypertrophy and its etiology. Murine models with excessive <jats:styled-content style=\"fixed-case\">TES<\/jats:styled-content> expression specific to the heart were constructed with an adeno\u2010associated virus expression system. Cardiac hypertrophy was stimulated through aortic banding (<jats:styled-content style=\"fixed-case\">AB<\/jats:styled-content>). The severity of cardiac hypertrophy was evaluated through molecular, echocardiographic, pathological, and hemodynamic examination. The findings of our study revealed that <jats:styled-content style=\"fixed-case\">TES<\/jats:styled-content> expression was remarkably suppressed not only in failing human hearts but also in mouse hearts with cardiac hypertrophy. It was discovered that excessive <jats:styled-content style=\"fixed-case\">TES<\/jats:styled-content> expression driven by an adeno\u2010associated viral vector noticeably inhibited hypertrophy triggered by angiotensin <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content> (Ang <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>) in cultivated cardiomyocytes from newborn rats. It was also revealed that <jats:styled-content style=\"fixed-case\">TES<\/jats:styled-content> knockdown via Adsh<jats:styled-content style=\"fixed-case\">TES<\/jats:styled-content> caused the reverse phenotype in cardiomyocytes. Furthermore, it was proved that excessive <jats:styled-content style=\"fixed-case\">TES<\/jats:styled-content> expression attenuated the ventricular dilation, cardiac hypertrophy, dysfunction, and fibrosis triggered by <jats:styled-content style=\"fixed-case\">AB<\/jats:styled-content> in mice. It was discovered that <jats:styled-content style=\"fixed-case\">TES<\/jats:styled-content> directly interacted with calcineurin and suppressed its downstream signalling pathway. Moreover, the inactivation of calcineurin with cyclosporin A greatly offset the exacerbated hypertrophic response triggered by <jats:styled-content style=\"fixed-case\">AB<\/jats:styled-content> in <jats:styled-content style=\"fixed-case\">TES<\/jats:styled-content> knockdown mice. Overall, the findings of our study suggest that <jats:styled-content style=\"fixed-case\">TES<\/jats:styled-content> serves as a crucial regulator of the hypertrophic reaction by hindering the calcineurin\u2010dependent pathway in the heart.<\/jats:p>","DOI":"10.1111\/jcmm.13934","type":"journal-article","created":{"date-parts":[[2018,11,23]],"date-time":"2018-11-23T08:56:06Z","timestamp":1542963366000},"page":"328-339","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Testin protects against cardiac hypertrophy by targeting a calcineurin\u2010dependent signalling pathway"],"prefix":"10.1111","volume":"23","author":[{"given":"Lu","family":"Gao","sequence":"first","affiliation":[{"name":"Department of Cardiology The First Affiliated Hospital of Zhengzhou University Zhengzhou 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