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Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
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Hdac9 inhibits medial artery calcification through down-regulation of Osterix

Pengcheng He1, Hongjiao Yu2, Lei Jiang1

  • 1Department of Cardiology, Guangdong Cardiovascular Institute, Guangdong Provincial Key Laboratory of Coronary Heart Disease Prevention, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou 510100, China.

Vascular Pharmacology
|July 24, 2020
PubMed

Insights

Histone deacetylase 9 (Hdac9) inhibits medial artery calcification (MAC) in chronic kidney disease (CKD) models. Down-regulation of Hdac9 promotes VSMC calcification, suggesting Hdac9 as a therapeutic target for MAC in CKD.

Area of Science:

  • Vascular Biology
  • Mineral Metabolism
  • Genetics

Background:

  • Medial artery calcification (MAC) is a major contributor to cardiovascular mortality in chronic kidney disease (CKD).
  • Genetic variants in histone deacetylase 9 (Hdac9) are linked to cardiovascular disease, but its role in CKD-related MAC is unknown.

Purpose of the Study:

  • To investigate the role of Hdac9 in vascular smooth muscle cell (VSMC) calcification and MAC in a CKD context.

Main Methods:

  • Induced MAC and VSMC calcification in mice using high phosphate and vitamin D3.
  • Assessed Hdac9 expression, calcium deposition, and Akt signaling pathways.
  • Utilized Hdac9 knockdown and overexpression models in VSMCs.

Main Results:

  • Hdac9 expression decreased during high phosphate-induced VSMC calcification and MAC.
  • Hdac9 knockdown exacerbated calcium deposition, while Hdac9 overexpression inhibited it.
  • Hdac9's anti-calcific effect was mediated by down-regulating Osterix, involving Akt signaling.

Conclusions:

  • Hdac9 acts as a novel inhibitor of medial artery calcification.
  • Hdac9 represents a potential therapeutic target for managing MAC in CKD patients.
Abstract

Keywords:
Chronic kidney diseaseHdac9Medial artery calcificationOsterixVascular smooth muscle cell

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