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  11. Gdf10 Is A Negative Regulator Of Vascular Calcification

GDF10 is a negative regulator of vascular calcification

Khrystyna Platko1, Gabriel Gyulay1, Paul F Lebeau1

  • 1Department of Medicine, Division of Nephrology, McMaster University, and The Research Institute of St Joe's Hamilton, Hamilton, Ontario, Canada.

The Journal of Biological Chemistry
|September 22, 2024

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View abstract on PubMed

Summary
This summary is machine-generated.

Growth differentiation factor 10 (GDF10) inhibits vascular calcification (VC) by preventing osteogenic transdifferentiation of vascular smooth muscle cells (VSMCs). Elevated GDF10 in chronic kidney disease patients with severe VC suggests its potential as a biomarker and therapeutic target.

Area of Science:

  • Cardiovascular Biology
  • Mineral Metabolism
  • Vascular Biology

Background:

  • Vascular calcification (VC) is a hallmark of cardiovascular disease in chronic kidney disease (CKD) patients.
  • VC involves osteogenic transdifferentiation of vascular smooth muscle cells (VSMCs), a process similar to bone formation.
  • Previous work showed loss of T-cell death-associated gene 51 (TDAG51) attenuates VC.

Purpose of the Study:

  • To investigate the role of growth differentiation factor 10 (GDF10) in the osteogenic transdifferentiation of VSMCs.
  • To determine if GDF10 can be a therapeutic target for vascular calcification.

Main Methods:

  • Primary mouse and human VSMCs and ex vivo aortic ring cultures were used.
  • Recombinant human GDF10 (rhGDF10) treatment and GDF10 knockout mouse models were employed.
Keywords:
bone morphogenic protein (BMP)calcificationcardiovascular diseasevascular biology

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  • In vivo studies and analysis of circulating GDF10 in CKD patients with severe VC were performed.

    • Main Results:

    • rhGDF10 treatment mitigated phosphate-induced hydroxyapatite (HA) deposition in VSMCs and aortic rings.
    • GDF10 knockout mice exhibited increased HA deposition.
    • rhGDF10 reduced runt-related transcription factor 2 expression, a key driver of VSMC osteogenic transdifferentiation.
    • In vivo rhGDF10 administration attenuated vitamin D3-induced VC.
    • Circulating GDF10 levels were elevated in CKD patients with severe VC.

    Conclusions:

    • GDF10 acts as an inhibitor of vascular calcification by suppressing VSMC osteogenic transdifferentiation.
    • GDF10 represents a potential novel biomarker for severe VC in CKD patients.
    • GDF10 may serve as a therapeutic target for managing vascular calcification.
    vascular smooth muscle cells