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Enhancer of Zeste Homologue 2 Promotes Vascular Calcification Associated With Chronic Kidney Disease
Pinglan Lin1,2,3, Yufeng Xing1,2,3, Ming Wu1,2,3
1Department of Nephrology, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, 201203 Shanghai, China.
Frontiers in Bioscience (Landmark Edition)
|April 29, 2026
Summary
Enhancer of Zeste Homologue 2 (EZH2) is elevated in vascular calcification associated with chronic kidney disease (CKD). Inhibiting EZH2 may offer a therapeutic strategy to treat CKD-related vascular calcification.
Area of Science:
- Vascular Biology
- Epigenetics
- Nephrology
Background:
- Vascular calcification (VC) is a major complication of chronic kidney disease (CKD).
- The epigenetic regulator Enhancer of Zeste Homologue 2 (EZH2) plays a role in kidney disorders.
- Understanding EZH2's role in CKD-associated VC is crucial.
Purpose of the Study:
- To investigate the role of EZH2 in the development of vascular calcification in CKD.
- To examine EZH2 expression levels in calcified vascular tissues from CKD patients and preclinical models.
Main Methods:
- Analysis of radial arteries from kidney failure patients.
- Establishment of CKD-associated VC mouse models and ex vivo/in vitro calcification models.
- Inhibition of EZH2 using 3-deazaneplanocin A (3-DZNeP) and modulation of EZH2/BMP2 expression.
Main Results:
- EZH2 expression was significantly higher in calcified arteries from CKD patients and preclinical models.
- High phosphate levels increased EZH2 and H3K27me3, promoting osteogenic markers and VSMC calcification.
- Overexpression of EZH2 aggravated VSMC calcification by upregulating bone morphogenetic protein (BMP) 2.
Conclusions:
- EZH2 is upregulated in vascular calcification associated with CKD.
- EZH2 promotes VC, potentially through BMP2 signaling.
- Targeting EZH2 represents a potential therapeutic approach for CKD-associated VC.
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