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Updated: Jun 14, 2026

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
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Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation

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Targeting B7-H3 attenuates uremic vascular calcification by suppressing phenotypic switching of VSMCs and regulating

Yansheng Jin1, Lan Ding1, Shuaishuai Gu1

  • 1Department of Nephrology and Immunology, Suzhou Wuzhong People's Hospital, Dongwu North Road, 61, Suzhou, 215128, Jiangsu, China.

Clinical and Experimental Nephrology
|January 4, 2026
PubMed
Abstract

Insights

B7-H3 promotes uremic vascular calcification by driving vascular smooth muscle cell (VSMC) osteogenic changes and enhancing pro-calcific macrophage recruitment. Targeting B7-H3 offers a potential therapeutic strategy for UVC.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Nephrology

Background:

  • Uremic vascular calcification (UVC) is a significant complication in chronic kidney disease.
  • B7-H3, an immune checkpoint molecule, is implicated in inflammation and vascular remodeling.
  • The specific role of B7-H3 in UVC pathogenesis remains unclear.

Purpose of the Study:

  • To investigate the role of B7-H3 in UVC.
  • To determine B7-H3's effects on calcium deposition and VSMC phenotype.
  • To elucidate B7-H3's influence on VSMC-macrophage crosstalk in UVC.

Main Methods:

  • Established an in vitro UVC model using human aortic VSMCs treated with β-glycerophosphate.
  • Utilized siRNA to silence B7-H3 expression.
  • Assessed calcification, VSMC phenotype markers, and macrophage recruitment, adhesion, and polarization (M1/M2) via co-culture systems, qRT-PCR, and flow cytometry.

Main Results:

  • β-GP induced VSMC calcification and upregulated B7-H3 expression.
  • B7-H3 silencing attenuated calcification, restored VSMC contractile markers, and reduced osteogenic markers.
  • B7-H3 knockdown suppressed macrophage recruitment and M1 polarization, favoring the M2 phenotype, and mitigated M1 macrophage-induced VSMC calcification.

Conclusions:

  • B7-H3 directly promotes UVC by inducing VSMC osteogenic transformation.
  • B7-H3 indirectly promotes UVC by enhancing macrophage recruitment and M1 polarization.
  • Targeting B7-H3 presents a promising therapeutic avenue for mitigating UVC.
Keywords:
B7-H3Osteogenic transdifferentiationUremiaVascular calcificationVascular smooth muscle cells

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