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  11. Histone Deacetylase 9 Promotes Osteogenic Trans-differentiation Of Vascular Smooth Muscle Cells Via Ferroptosis In Chronic Kidney Disease Vascular Calcification

Histone deacetylase 9 promotes osteogenic trans-differentiation of vascular smooth muscle cells via ferroptosis in chronic kidney disease vascular calcification

Lin Xiong1, Qiong Xiao1, Rong Chen1

  • 1Department of Nephrology and Institute of Nephrology, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Sichuan Clinical Research Centre for Kidney Diseases, Clinical Immunology Translational Medicine Key Laboratory of Sichuan Province, Chengdu, China.

Renal Failure
|November 5, 2024

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View abstract on PubMed

Summary
This summary is machine-generated.

Histone deacetylase 9 (HDAC9) drives vascular calcification in chronic kidney disease (CKD) by promoting smooth muscle cell trans-differentiation and ferroptosis. Inhibiting HDAC9 may offer a new therapeutic strategy for CKD vascular complications.

Area of Science:

  • Cardiovascular Biology
  • Nephrology
  • Cellular Biology

Background:

  • Vascular calcification is a significant complication of chronic kidney disease (CKD).
  • The trans-differentiation of vascular smooth muscle cells (VSMCs) into osteoblast-like cells is a key process in CKD vascular calcification.
  • While ferroptosis is implicated, its regulatory mechanisms in CKD vascular calcification are not fully understood.

Purpose of the Study:

  • To investigate the regulatory mechanism of ferroptosis in CKD vascular calcification.
  • To explore the role of Histone deacetylase 9 (HDAC9) in this process.

Main Methods:

  • Transcriptome sequencing was used to identify potential links between HDAC9 and ferroptosis.
  • HDAC9 expression was analyzed in human CKD patient arteries and a rat CKD model.
Keywords:
HDAC9ferroptosisosteogenic trans-differentiationvascular calcification

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  • HDAC9 knockout and RSL3 (a ferroptosis inducer) treatments were used to assess effects on VSMC osteogenic trans-differentiation and ferroptosis.

    • Main Results:

    • Transcriptome sequencing suggested a relationship between HDAC9 and ferroptosis in CKD vascular calcification.
    • Increased HDAC9 expression was observed in calcified arteries from CKD patients and a rat model.
    • HDAC9 knockout attenuated high calcium/phosphorus-induced osteogenic trans-differentiation and ferroptosis in VSMCs.
    • RSL3 exacerbated these effects, which were partially suppressed by HDAC9 knockout.

    Conclusions:

    • HDAC9 promotes VSMC osteogenic trans-differentiation and ferroptosis in the context of CKD.
    • HDAC9 represents a potential therapeutic target for mitigating vascular calcification in CKD.
    vascular smooth muscle cell