ArticleInternational journal of molecular sciences2025
Regulation of Vascular Calcification by M1-Type Macrophage-Derived Semaphorin 4D.
Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Joint association of systemic inflammatory response index and thromboelastography maximum amplitude with the risk of early atherosclerosis in patients with rheumatoid arthritis.Clinical and experimental medicine · 2026Article
- Immune mechanisms in chronic kidney disease-mineral and bone disorder: current insights and therapeutic implications.Frontiers in medicine · 2025Review
- Construction of a diagnostic model and identification of effect genes for diabetic kidney disease with concurrent vascular calcification based on bioinformatics and multiple machine learning approaches.Frontiers in molecular biosciences · 2025Article
- The role of macrophages in vascular calcification: strategies for diagnosis and treatment.Frontiers in immunology · 2025Review
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Authors and funding
6 authors.
Funding
Abstract
Vascular calcification is a critical pathological hallmark of cardiovascular diseases. Although previous studies have indicated that M1 macrophages significantly promote calcification, the exact underlying mechanisms remain unclear. This study examined whether semaphorin 4D (Sema4D), a class IV semaphorin involved in atherosclerosis development, is secreted by M1 macrophages and contributes to the calcification of vascular smooth muscle cells (VSMCs). We observed elevated expression and secretion of Sema4D in both M1 and M2 macrophages, with significantly higher levels in M1-polarized cells. M1 macrophages promoted VSMC calcification in both co-culture and conditioned medium systems, as evidenced by increased alkaline phosphatase activity, enhanced calcium deposition, and upregulation of osteogenic markers. Notably, neutralization of Sema4D in M1 conditioned medium using pepinemab, an anti-Sema4D antibody, effectively attenuated VSMC calcification induced by M1 macrophages. Conversely, supplementation of conditioned medium with recombinant Sema4D enhanced calcification and osteogenic signaling in VSMCs, further supporting the pro-calcifying role of Sema4D. Collectively, these findings highlight macrophage-derived Sema4D as a pivotal regulator of vascular calcification and a promising therapeutic target.
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Registered trials
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