title: Activation of TRPV1 attenuates high salt-induced cardiac hypertrophy through improvement of mitochondrial function.
abstract: OBJECTIVE
  High-salt diet induces cardiac remodelling and leads to heart failure, which is closely related to cardiac mitochondrial dysfunction. Transient receptor potential (TRP) channels are implicated in the pathogenesis of cardiac dysfunction. We investigated whether activation of TRP vanilloid (subtype 1) (TRPV1) channels by dietary capsaicin can, by ameliorating cardiac mitochondrial dysfunction, prevent high-salt diet-induced cardiac hypertrophy.
  
  
  METHODS
  Male wild-type (WT) and TRPV1(-/-) mice were fed a normal or high-salt 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-resolution respirometry. The expression levels of TRPV1, sirtuin 3 and NDUFA9 were detected in cardiac cells and tissues.
  
  
  RESULTS
  Chronic high-salt diet caused cardiac hypertrophy and reduced physical activity in mice; both effects were ameliorated by capsaicin intake in WT but not in TRPV1(-/-) mice. TRPV1 knockout or high-salt diet significantly jeopardized the proficiency of mitochondrial Complex I oxidative phosphorylation (OXPHOS) and reduced Complex I enzyme activity. Chronic dietary capsaicin increased cardiac mitochondrial sirtuin 3 expression, the proficiency of Complex I OXPHOS, ATP production and Complex I enzyme activity in a TRPV1-dependent manner.
  
  
  CONCLUSIONS
  TRPV1 activation by dietary capsaicin can antagonize high-salt diet-mediated cardiac lesions by ameliorating its deleterious effect on the proficiency of Complex I OXPHOS. TRPV1-mediated amendment of mitochondrial dysfunction may represent a novel target for management of early cardiac dysfunction.
authors.affiliation: Center for Hypertension and Metabolic Diseases, Department of Hypertension and Endocrinology, Daping Hospital, Third Military Medical University, Chongqing Institute of Hypertension, Chongqing, China.
authors.forename: Hongmei
authors.initials: H
authors.lastname: Lang
authors.affiliation: Center for Hypertension and Metabolic Diseases, Department of Hypertension and Endocrinology, Daping Hospital, Third Military Medical University, Chongqing Institute of Hypertension, Chongqing, China.
authors.forename: Qiang
authors.initials: Q
authors.lastname: Li
authors.affiliation: Center for Hypertension and Metabolic Diseases, Department of Hypertension and Endocrinology, Daping Hospital, Third Military Medical University, Chongqing Institute of Hypertension, Chongqing, China.
authors.forename: Hao
authors.initials: H
authors.lastname: Yu
authors.affiliation: Department of Cardiology, Affiliated Hospital of Zunyi Medical College, Institute of Clinical Medicine of Zunyi Medical College, Zunyi, Guizhou, China.
authors.forename: Peng
authors.initials: P
authors.lastname: Li
authors.affiliation: Center for Hypertension and Metabolic Diseases, Department of Hypertension and Endocrinology, Daping Hospital, Third Military Medical University, Chongqing Institute of Hypertension, Chongqing, China.
authors.forename: Zongshi
authors.initials: Z
authors.lastname: Lu
authors.affiliation: Center for Hypertension and Metabolic Diseases, Department of Hypertension and Endocrinology, Daping Hospital, Third Military Medical University, Chongqing Institute of Hypertension, Chongqing, China.
authors.forename: Shiqiang
authors.initials: S
authors.lastname: Xiong
authors.affiliation: Center for Hypertension and Metabolic Diseases, Department of Hypertension and Endocrinology, Daping Hospital, Third Military Medical University, Chongqing Institute of Hypertension, Chongqing, China.
authors.forename: Tao
authors.initials: T
authors.lastname: Yang
authors.affiliation: Center for Hypertension and Metabolic Diseases, Department of Hypertension and Endocrinology, Daping Hospital, Third Military Medical University, Chongqing Institute of Hypertension, Chongqing, China.
authors.forename: Yu
authors.initials: Y
authors.lastname: Zhao
authors.affiliation: Center for Hypertension and Metabolic Diseases, Department of Hypertension and Endocrinology, Daping Hospital, Third Military Medical University, Chongqing Institute of Hypertension, Chongqing, China.
authors.forename: Xiaohu
authors.initials: X
authors.lastname: Huang
authors.affiliation: Center for Hypertension and Metabolic Diseases, Department of Hypertension and Endocrinology, Daping Hospital, Third Military Medical University, Chongqing Institute of Hypertension, Chongqing, China.
authors.forename: Peng
authors.initials: P
authors.lastname: Gao
authors.affiliation: Center for Hypertension and Metabolic Diseases, Department of Hypertension and Endocrinology, Daping Hospital, Third Military Medical University, Chongqing Institute of Hypertension, Chongqing, China.
authors.forename: Hexuan
authors.initials: H
authors.lastname: Zhang
authors.affiliation: Department of Cardiology, Affiliated Hospital of Zunyi Medical College, Institute of Clinical Medicine of Zunyi Medical College, Zunyi, Guizhou, China.
authors.forename: Qianhui
authors.initials: Q
authors.lastname: Shang
authors.affiliation: Center for Hypertension and Metabolic Diseases, Department of Hypertension and Endocrinology, Daping Hospital, Third Military Medical University, Chongqing Institute of Hypertension, Chongqing, China.
authors.forename: Daoyan
authors.initials: D
authors.lastname: Liu
authors.affiliation: Center for Hypertension and Metabolic Diseases, Department of Hypertension and Endocrinology, Daping Hospital, Third Military Medical University, Chongqing Institute of Hypertension, Chongqing, China.
authors.forename: Zhiming
authors.initials: Z
authors.lastname: Zhu
mesh_terms: D000818:Animals; D006332:Cardiomegaly / Q000139:chemically induced* / Q000473:pathology / Q000517:prevention & control*; D002478:Cells, Cultured; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008929:Mitochondria, Heart / Q000187:drug effects*; D051381:Rats; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage / Q000494:pharmacology*; D050916:TRPV Cation Channels / Q000819:agonists* / Q000172:deficiency
chemical_list: D017673:Sodium Chloride, Dietary; D050916:TRPV Cation Channels; C493921:TRPV1 protein, mouse