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High\u2010mobility group box 1 (<jats:styled-content style=\"fixed-case\">HMGB<\/jats:styled-content>1), which is increased in myocardium under pressure overload, may be involved in pressure overload\u2010induced cardiac injury. The objectives of this study are to determine the role of <jats:styled-content style=\"fixed-case\">HMGB<\/jats:styled-content>1 in cardiac hypertrophy and cardiac dysfunction under pressure overload. Pressure overload was imposed on the heart of male wild\u2010type mice by transverse aortic constriction (<jats:styled-content style=\"fixed-case\">TAC<\/jats:styled-content>), while recombinant <jats:styled-content style=\"fixed-case\">HMGB<\/jats:styled-content>1, <jats:styled-content style=\"fixed-case\">HMGB<\/jats:styled-content>1 box A (a competitive antagonist of <jats:styled-content style=\"fixed-case\">HMGB<\/jats:styled-content>1) or <jats:styled-content style=\"fixed-case\">PBS<\/jats:styled-content> was injected into the <jats:styled-content style=\"fixed-case\">LV<\/jats:styled-content> wall. Moreover, cardiac myocytes were cultured and given sustained mechanical stress. Transthoracic echocardiography was performed after the operation and sections for histological analyses were generated from paraffin\u2010embedded hearts. Relevant proteins and genes were detected. Cardiac <jats:styled-content style=\"fixed-case\">HMGB<\/jats:styled-content>1 expression was increased after <jats:styled-content style=\"fixed-case\">TAC<\/jats:styled-content>, which was accompanied by its translocation from nucleus to both cytoplasm and intercellular space. Exogenous <jats:styled-content style=\"fixed-case\">HMGB<\/jats:styled-content>1 aggravated <jats:styled-content style=\"fixed-case\">TAC<\/jats:styled-content>\u2010induced cardiac hypertrophy and cardiac dysfunction, as demonstrated by echocardiographic analyses, histological analyses and foetal cardiac genes detection. Nevertheless, the aforementioned pathological change induced by <jats:styled-content style=\"fixed-case\">TAC<\/jats:styled-content> could partially be reversed by <jats:styled-content style=\"fixed-case\">HMGB<\/jats:styled-content>1 inhibition. Consistent with the <jats:italic>in vivo<\/jats:italic> observations, mechanical stress evoked the release and synthesis of <jats:styled-content style=\"fixed-case\">HMGB<\/jats:styled-content>1 in cultured cardiac myocytes. This study indicates that the activated and up\u2010regulated <jats:styled-content style=\"fixed-case\">HMGB<\/jats:styled-content>1 in myocardium, which might partially be derived from cardiac myocytes under pressure overload, may be of crucial importance in pressure overload\u2010induced cardiac hypertrophy and cardiac dysfunction.<\/jats:p>","DOI":"10.1111\/jcmm.12743","type":"journal-article","created":{"date-parts":[[2015,12,10]],"date-time":"2015-12-10T10:05:23Z","timestamp":1449741923000},"page":"459-470","source":"Crossref","is-referenced-by-count":38,"title":["Extracellular high\u2010mobility group box 1 mediates pressure overload\u2010induced cardiac hypertrophy and heart failure"],"prefix":"10.1111","volume":"20","author":[{"given":"Lei","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Cardiology Shanghai Institute of Cardiovascular Diseases Zhongshan Hospital Shanghai Medical College of Fudan University Shanghai 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