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Related Experiment Video

Updated: Apr 17, 2026

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
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E3 Ubiquitin Ligase RNF10 Negatively Regulates Rbpjk Expression During Vascular Calcification in Chronic Kidney

Guiquan Yu1, Bin Tang1, Jingyang Ran1

  • 1Department of Nephrology, The Second Affiliated Hospital of Chongqing Medical University, China (G.Y., B.T., J.R., S.X., Q.C., P.Y., C.W., G.W., Z.Z., X.L.).

Arteriosclerosis, Thrombosis, and Vascular Biology
|April 16, 2026
PubMed
Summary

Reduced RNF10 levels trigger vascular calcification in chronic kidney disease by upregulating Rbpjk. RNF10 protects against calcification via Rbpjk regulation, not its E3 ligase activity, offering new therapeutic targets.

Keywords:
muscle, smooth, vascularratsrenal insufficiency, chronicubiquitin-protein ligasesvascular calcification

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Nephrology

Background:

  • Vascular calcification is common in chronic kidney disease (CKD), with vascular smooth muscle cells (VSMCs) playing a critical role.
  • The E3 ubiquitin ligase RNF10 (ring finger protein 10) is known to regulate VSMC proliferation and apoptosis.
  • The specific role of RNF10 in vascular calcification was previously uninvestigated.

Purpose of the Study:

  • To investigate the role of RNF10 in vascular calcification associated with chronic kidney disease.
  • To elucidate the underlying molecular mechanisms by which RNF10 influences vascular calcification.
  • To explore the potential of the RNF10-Rbpjk axis as a therapeutic target for vascular calcification.

Main Methods:

  • Assessed serum RNF10 levels in CKD patients with vascular calcification.
  • Evaluated RNF10 expression in calcified rat aortas and VSMCs.
  • Utilized Rnf10 knock-in rats and RNF10-overexpressed VSMCs to study RNF10's effects.
  • Employed RNA-seq, ChIP-seq, ChIP-qPCR, and luciferase assays to uncover molecular mechanisms.
  • Conducted gain- and loss-of-function experiments targeting Rbpjk in vitro and in vivo.

Main Results:

  • Lower circulating RNF10 levels and reduced RNF10 protein expression were observed in CKD patients and calcified rat aortas/VSMCs.
  • Rnf10 knock-in and RNF10 overexpression attenuated vascular calcification and reduced osteogenic marker expression.
  • RNF10 exerted protective effects independent of its E3 ubiquitin ligase activity, primarily through negative regulation of Rbpjk expression.

Conclusions:

  • RNF10 depletion initiates Rbpjk-driven osteogenic differentiation in CKD-associated vascular calcification.
  • The protective role of RNF10 is mediated by negative Rbpjk expression regulation, not its ubiquitin ligase function.
  • The identified RNF10-Rbpjk regulatory axis offers novel therapeutic strategies for vascular calcification.