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Transient receptor potential (TRP<\/jats:styled-content>) channels are implicated in the pathogenesis of cardiac dysfunction. We investigated whether activation of TRP<\/jats:styled-content> vanilloid (subtype 1) (TRPV1<\/jats:styled-content>) channels by dietary capsaicin can, by ameliorating cardiac mitochondrial dysfunction, prevent high\u2010salt diet\u2010induced cardiac hypertrophy.<\/jats:p><\/jats:sec>Experimental Approach<\/jats:title>Male wild\u2010type (WT<\/jats:styled-content>) and TRPV1<\/jats:styled-content>\u2212\/\u2212<\/jats:sup> mice were fed a normal or high\u2010salt diet with or without capsaicin for 6 months. Their cardiac parameters and endurance capacity were assessed. Mitochondrial respiration and oxygen consumption were measured using high\u2010resolution respirometry. The expression levels of TRPV<\/jats:styled-content>1, sirtuin 3 and NDUFA<\/jats:styled-content>9 were detected in cardiac cells and tissues.<\/jats:p><\/jats:sec>Key Results<\/jats:title>Chronic high\u2010salt diet caused cardiac hypertrophy and reduced physical activity in mice; both effects were ameliorated by capsaicin intake in WT<\/jats:styled-content> but not in TRPV1<\/jats:styled-content>\u2212\/\u2212<\/jats:sup> mice. TRPV1<\/jats:styled-content> knockout or high\u2010salt diet significantly jeopardized the proficiency of mitochondrial C<\/jats:styled-content>omplex I oxidative phosphorylation (OXPHOS<\/jats:styled-content>) and reduced Complex I enzyme activity. Chronic dietary capsaicin increased cardiac mitochondrial sirtuin 3 expression, the proficiency of C<\/jats:styled-content>omplex I OXPHOS<\/jats:styled-content>, ATP<\/jats:styled-content> production and C<\/jats:styled-content>omplex I enzyme activity in a TRPV1<\/jats:styled-content>\u2010dependent manner.<\/jats:p><\/jats:sec>Conclusions and Implications<\/jats:title>TRPV1<\/jats:styled-content> activation by dietary capsaicin can antagonize high\u2010salt diet\u2010mediated cardiac lesions by ameliorating its deleterious effect on the proficiency of C<\/jats:styled-content>omplex I OXPHOS<\/jats:styled-content>. TRPV1<\/jats:styled-content>\u2010mediated amendment of mitochondrial dysfunction may represent a novel target for management of early cardiac dysfunction.<\/jats:p><\/jats:sec>Linked Articles<\/jats:title>This article is part of a themed section on Chinese Innovation in Cardiovascular Drug Discovery. To view the other articles in this section visit http:\/\/dx.doi.org\/10.1111\/bph.2015.172.issue-23<\/jats:ext-link><\/jats:p><\/jats:sec>","DOI":"10.1111\/bph.12987","type":"journal-article","created":{"date-parts":[[2014,10,23]],"date-time":"2014-10-23T04:29:50Z","timestamp":1414038590000},"page":"5548-5558","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":79,"title":["Activation of TRPV1<\/scp> attenuates high salt\u2010induced cardiac hypertrophy through improvement of mitochondrial function"],"prefix":"10.1111","volume":"172","author":[{"given":"Hongmei","family":"Lang","sequence":"first","affiliation":[{"name":"Center for Hypertension and Metabolic Diseases, Department of Hypertension and Endocrinology, Daping Hospital Third Military Medical University, Chongqing Institute of Hypertension Chongqing 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