ArticleClinical and experimental nephrology2026
Targeting B7-H3 attenuates uremic vascular calcification by suppressing phenotypic switching of VSMCs and regulating VSMCs-macrophage crosstalk.
Article in Clinical and experimental nephrology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveThis study aimed to investigate the role of B7-H3-an immune checkpoint implicated in inflammation and vascular remodeling-in uremic vascular calcification (UVC), particularly its effects on calcium deposition, vascular smooth muscle cell (VSMC) phenotype, and VSMC-macrophage crosstalk.
methodsAn in vitro UVC model was established using β-glycerophosphate (β-GP) treated human aortic VSMCs (HA-VSMCs). B7-H3 expression was silenced using siRNA. Calcification was assessed by Alizarin Red S staining, ALP activity, and calcium content assays. VSMCs phenotype switching was evaluated by Western blot for contractile and osteogenic markers. Macrophage recruitment, adhesion, and polarization (M1/M2) were assessed using THP-1 cells in co-culture systems and analyzed by qRT-PCR and flow cytometry. The effect of macrophage polarization on VSMCs calcification was investigated in the presence or absence of B7-H3 knockdown.
resultsβ-GP treatment induced HA-VSMC calcification, osteogenic differentiation, and upregulated B7-H3 expression. Silencing B7-H3 attenuated calcification, restored contractile markers, and reduced osteogenic markers in VSMCs. B7-H3 knockdown also suppressed the recruitment and adhesion of macrophages to HA-VSMCs, inhibited M1 polarization of co-cultured macrophages, and promoted their shift toward the M2 phenotype. Furthermore, silencing B7-H3 mitigated M1 macrophage-induced VSMC calcification and enhanced the protective effects of M2 macrophages.
conclusionB7-H3 promotes UVC directly by inducing osteogenic transformation of VSMCs and indirectly by enhancing macrophage recruitment and favoring pro-calcific M1 polarization. Thus, targeting B7-H3 may represent a promising therapeutic strategy to mitigate UVC.
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