ArticleScientific reports2024
C5a-C5AR1 axis as a potential trigger of the rupture of intracranial aneurysms.
Article in Scientific reports, 2024. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 3 citations in OpenAlex.
- Achievement and Future Prospectives from Translational Research Targeting Intracranial Aneurysm.Neurologia medico-chirurgica · 2026Review
- Single-cell and spatial transcriptomics analysis of osteoarthritis: pathway regulation, cell interaction networks, and therapeutic translation.Journal of translational medicine · 2026Review
- Mechanisms of Intracranial Aneurysm Rupture: An Integrative Review of Experimental and Clinical Evidence.Journal of clinical medicine · 2025Review
- Dual role of complement in neuronal repair.Frontiers in immunology · 2025Review
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
Abstract
Recent studies have indicated the involvement of neutrophil-mediated inflammatory responses in the process leading to intracranial aneurysm (IA) rupture. Receptors mediating neutrophil recruitment could thus be therapeutic targets of unruptured IAs. In this study, complement C5a receptor 1 (C5AR1) was picked up as a candidate that may cause neutrophil-dependent inflammation in IA lesions from comprehensive gene expression profile data acquired from rat and human samples. The induction of C5AR1 in IA lesions was confirmed by immunohistochemistry; the up-regulations of C5AR1/C5ar1 stemmed from infiltrated neutrophils, which physiologically express C5AR1/C5ar1, and adventitial fibroblasts that induce C5AR1/C5ar1 in human/rat IA lesions. In in vitro experiments using NIH/3T3, a mouse fibroblast-like cell line, induction of C5ar1 was demonstrated by starvation or pharmacological inhibition of mTOR signaling by Torin1. Immunohistochemistry and an experiment in a cell-free system using recombinant C5 protein and recombinant Plasmin indicated that the ligand of C5AR1, C5a, could be produced through the enzymatic digestion by Plasmin in IA lesions. In conclusion, we have identified a potential contribution of the C5a-C5AR1 axis to neutrophil infiltration as well as inflammatory responses in inflammatory cells and fibroblasts of IA lesions. This cascade may become a therapeutic target to prevent the rupture of IAs.
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Registered trials
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