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The KLF7/PFKL/ACADL axis modulates cardiac metabolic remodelling during cardiac hypertrophy in male mice

Author

Listed:
  • Cao Wang

    (Harbin Institute of Technology)

  • Shupei Qiao

    (Harbin Medical University)

  • Yufang Zhao

    (Harbin Institute of Technology)

  • Hui Tian

    (Harbin Institute of Technology)

  • Wei Yan

    (The First Affiliated Hospital of Harbin Medical University)

  • Xiaolu Hou

    (The Fourth Affiliated Hospital of Harbin Medical University)

  • Ruiqi Wang

    (Harbin Institute of Technology)

  • Bosong Zhang

    (Harbin Institute of Technology)

  • Chaofan Yang

    (Harbin Institute of Technology)

  • Fuxing Zhu

    (Harbin Institute of Technology)

  • Yanwen Jiao

    (Harbin Institute of Technology)

  • Jiaming Jin

    (Harbin Institute of Technology)

  • Yue Chen

    (Harbin Institute of Technology)

  • Weiming Tian

    (Harbin Institute of Technology)

Abstract

The main hallmark of myocardial substrate metabolism in cardiac hypertrophy or heart failure is a shift from fatty acid oxidation to greater reliance on glycolysis. However, the close correlation between glycolysis and fatty acid oxidation and underlying mechanism by which causes cardiac pathological remodelling remain unclear. We confirm that KLF7 simultaneously targets the rate-limiting enzyme of glycolysis, phosphofructokinase-1, liver, and long-chain acyl-CoA dehydrogenase, a key enzyme for fatty acid oxidation. Cardiac-specific knockout and overexpression KLF7 induce adult concentric hypertrophy and infant eccentric hypertrophy by regulating glycolysis and fatty acid oxidation fluxes in male mice, respectively. Furthermore, cardiac-specific knockdown phosphofructokinase-1, liver or overexpression long-chain acyl-CoA dehydrogenase partially rescues the cardiac hypertrophy in adult male KLF7 deficient mice. Here we show that the KLF7/PFKL/ACADL axis is a critical regulatory mechanism and may provide insight into viable therapeutic concepts aimed at the modulation of cardiac metabolic balance in hypertrophied and failing heart.

Suggested Citation

  • Cao Wang & Shupei Qiao & Yufang Zhao & Hui Tian & Wei Yan & Xiaolu Hou & Ruiqi Wang & Bosong Zhang & Chaofan Yang & Fuxing Zhu & Yanwen Jiao & Jiaming Jin & Yue Chen & Weiming Tian, 2023. "The KLF7/PFKL/ACADL axis modulates cardiac metabolic remodelling during cardiac hypertrophy in male mice," Nature Communications, Nature, vol. 14(1), pages 1-18, December.
    • Handle: RePEc:nat:natcom:v:14:y:2023:i:1:d:10.1038_s41467-023-36712-9
    DOI: 10.1038/s41467-023-36712-9
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    References listed on IDEAS

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    1. Atsushi Hoshino & Wei-jia Wang & Shogo Wada & Chris McDermott-Roe & Chantell S. Evans & Bridget Gosis & Michael P. Morley & Komal S. Rathi & Jian Li & Kristina Li & Steven Yang & Meagan J. McManus & C, 2019. "The ADP/ATP translocase drives mitophagy independent of nucleotide exchange," Nature, Nature, vol. 575(7782), pages 375-379, November.
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    3. Le Li & Lijia Li & Wei Li & Taiqi Chen & Bin Zou & Lina Zhao & Huili Wang & Xueying Wang & Lina Xu & Xiaohui Liu & Dong Wang & Bo Li & Tak W. Mak & Wenjing Du & Xiaolu Yang & Peng Jiang, 2018. "TAp73-induced phosphofructokinase-1 transcription promotes the Warburg effect and enhances cell proliferation," Nature Communications, Nature, vol. 9(1), pages 1-13, December.
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