PUBLICATION

ndufa7 plays a critical role in cardiac hypertrophy

Authors
Shi, X., Zhang, Y., Chen, R., Gong, Y., Zhang, M., Guan, R., Rotstein, O.D., Liu, X., Wen, X.Y.
ID
ZDB-PUB-201002-204
Date
2020
Source
Journal of Cellular and Molecular Medicine   24(22): 13151-13162 (Journal)
Registered Authors
Wen, Xiao-Yan, Zhang, Yu
Keywords
ndufa7, cardiac hypertrophy, nppa, nppb, zebrafish
MeSH Terms
  • Signal Transduction
  • Animals
  • Zebrafish/embryology
  • Zebrafish/metabolism
  • Heart Failure/metabolism
  • Biomarkers/metabolism
  • Calcineurin/metabolism
  • Reactive Oxygen Species/metabolism
  • Gene Knockdown Techniques
  • Disease Models, Animal
  • Cardiomyopathy, Hypertrophic/enzymology
  • Cardiomyopathy, Hypertrophic/pathology*
  • Arteries/metabolism
  • Tissue Distribution
  • Electron Transport Complex I/metabolism*
  • Cell Line
  • Cardiomegaly/enzymology
  • Cardiomegaly/pathology*
  • Mice
  • Hypertension/metabolism
  • Heart/physiopathology
  • Genotype
(all 22)
PubMed
32989924 Full text @ J. Cell. Mol. Med.
Abstract
Cardiac hypertrophy is a common pathological change in patients with progressive cardiac function failure, which can be caused by hypertrophic cardiomyopathy (HCM), dilated cardiomyopathy (DCM) or arterial hypertension. Despite years of study, there is still limited knowledge about the underlying molecular mechanisms for cardiac hypertrophy. NDUFA7, a subunit of NADH:ubiquinone oxidoreductase (complex I), has been reported to be a novel HCM associated gene. However, the biological role of NDUFA7 in heart remains unknown. In this study, we found that NDUFA7 exhibited high expression in the heart, and its level was significantly decreased in mice model of cardiac hypertrophy. Moreover, we demonstrated that ndufa7 knockdown in developing zebrafish embryos resulted in cardiac development and functional defects, associated with increased expression of pathological hypertrophy biomarkers nppa (ANP) and nppb (BNP). Mechanistic study demonstrated that ndufa7 depletion promoted ROS production and calcineurin signalling activation. Moreover, NDUFA7 depletion contributed to cardiac cell hypertrophy. Together, these results report for the first time that ndufa7 is implicated in pathological cardiac hypertrophy.
Genes / Markers
Figures
Figure Gallery (6 images)
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Expression
Phenotype
Mutations / Transgenics
Allele Construct Type Affected Genomic Region
twu34TgTransgenic Insertion
    zf3504TgTransgenic Insertion
      1 - 2 of 2
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      Human Disease / Model
      1 - 1 of 1
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      Sequence Targeting Reagents
      Target Reagent Reagent Type
      ndufa7MO1-ndufa7MRPHLNO
      1 - 1 of 1
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      Fish
      Antibodies
      Name Type Antigen Genes Isotypes Host Organism
      Ab1-ndufa7polyclonal
        IgGGoat
        1 - 1 of 1
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        Orthology
        Gene Orthology
        ndufa7
        1 - 1 of 1
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        Engineered Foreign Genes
        Marker Marker Type Name
        EGFPEFGEGFP
        LuciferaseEFGLuciferase
        1 - 2 of 2
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        Mapping
        No data available