ArticleFrontiers in immunology2025
Ninjurin-1 drives atherosclerosis progression via
Article in Frontiers in immunology, 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.
- Ninjurin1 in cardiovascular and vascular biology: From molecular mechanisms to therapeutic opportunities.Clinical and translational medicine · 2026Review
- Delving into pyroptosis in atherosclerosis: role, mechanisms and therapeutic opportunities.Frontiers in immunology · 2026Review
- Research Progress of Nerve Injury-Induced Protein 1 in Cardiovascular Diseases.Cardiology research and practice · 2026Review
- Synergistic effects of fecal microbiota transplantation and andrographolide on gut microbiota modulation in dextran sulfate sodium-induced colitis in mice.Frontiers in microbiology · 2026Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Atherosclerosis represents the leading cause of cardiovascular mortality, with persistent inflammation driving residual risk despite lipid-lowering therapies. While Ninjurin-1 (Ninj1) has been implicated in inflammatory diseases, its endothelial-specific role in atherosclerosis remains unclear. Methods: We conducted integrated molecular, functional, and histological analyses to characterize Ninj1 expression and function in atherosclerosis. Endothelial Ninj1 silencing was performed to assess its effects on NF-κB signaling, CXCL-8 expression, and ox-LDL-induced endothelial dysfunction. Results: Ninj1 silencing in endothelial cells suppressed NF-κB signaling and its key inflammatory mediator CXCL-8, conferring protection against ox-LDL-induced endothelial dysfunction by enhancing proliferation and migration while reducing apoptosis (all p < 0.05). In ApoE Discussion: Our results provide the first evidence that endothelial Ninj1 functions as a novel activator of the NF-κB/CXCL-8 axis, establishing its causal role in atherosclerosis and highlighting its potential as a targeted anti-inflammatory therapy.
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Registered trials
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