ArticleFrontiers in immunology2023
Axl promotes intracranial aneurysm rupture by regulating macrophage polarization toward M1
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- Remote Ischemic Post-Conditioning Preserves the Neurovascular Unit by Brain-Derived Gas6 That Drives Monocyte-Derived Macrophage Reprogramming via Axl and Vimentin after SAH.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The role of non-coding RNAs derived from macrophage exosomes in cardiovascular diseases.The Journal of physiology · 2026Review
- Integrated bioinformatics and experimental validation reveal that kaempferol ameliorates intervertebral disc degeneration via dual anti-inflammatory and anti-aging pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- LDHA protects vascular endothelial cells from oxidative stress‑induced mitochondrial damage via HIF‑1α activation and glycolytic reprogramming.Molecular medicine reports · 2026Article
- From hemodynamic stress to inflammatory wall remodeling in intracranial aneurysms.Frontiers in molecular biosciences · 2026Review
- Mechanisms of Intracranial Aneurysm Rupture: An Integrative Review of Experimental and Clinical Evidence.Journal of clinical medicine · 2025Review
- A Preliminary Study of Effect of Melatonin on Inflammation and Hypoxia-Related Factors in a Mouse Model of Elastase-Induced Intracranial Aneurysm.Brain and behavior · 2025Article
- AXL: shapers of tumor progression and immunosuppressive microenvironments.Molecular cancer · 2025Review
- tRF-AspGTC Promotes Intracranial Aneurysm Formation by Controlling TRIM29-Mediated Galectin-3 Ubiquitination.Research (Washington, D.C.) · 2025Article
- Research progress of HIF-1a on immunotherapy outcomes in immune vascular microenvironment.Frontiers in immunology · 2025Review
- SLC40A1-mediated positive feedback loop with M1 macrophages suppresses epithelial ovarian cancer progression.Frontiers in immunology · 2025Article
- WNTA5-mediated miR-374a-5p regulates vascular smooth muscle cell phenotype transformation and M1 macrophage polarization impacting intracranial aneurysm progression.Scientific reports · 2024Article
- The role of transcription factors in the pathogenesis and therapeutic targeting of vascular diseases.Frontiers in cardiovascular medicine · 2024Review
- Current understanding of macrophages in intracranial aneurysm: relevant etiological manifestations, signaling modulation and therapeutic strategies.Frontiers in immunology · 2023Review
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Macrophage infiltration and polarization are crucial for the pathogenesis of intracranial aneurysm (IA) rupture. Axl, a receptor tyrosine kinase, is involved in inflammation and efferocytosis in multiple organs. Upregulated soluble Axl in cerebrospinal fluid (CSF) and plasma is correlated with intracranial aneurysm rupture. This study aimed to investigate the role of Axl in IA rupture and macrophage polarization. Methods: Male C57BL/6J mice were used to induce IA. The level of Axl from control vessels and unruptured and ruptured IA samples was detected. In addition, the relationship between Axl and macrophages was confirmed. The pathway of Axl-mediated macrophage polarization was explored after IA induction Results: Compared with that in normal vessels, Axl expression was significantly upregulated in unruptured IA samples. The ruptured IA tissue exhibited significantly higher expression of Axl than the unruptured IA tissue. Axl and F4/80 were coexpressed in IA tissue and LPS/IFN-γ-stimulated BMDMs. R428 treatment significantly reduced the rate of M1-like macrophage infiltration and IA rupture. In contrast, rmGas6 treatment promoted M1 macrophage infiltration and IA rupture. Mechanistically, R428 inhibited the phosphorylation of Axl and STAT1 and the expression of hypoxia-inducible factor-1α (HIF-1α) and decreased the levels of IL-1β, NOS2, and MMP9 in LPS/IFN-γ-stimulated BMDMs. rmGas6 promoted the phosphorylation of Axl and STAT1 and the expression of HIF-1α. In addition, STAT1 knockdown abolished Axl-mediated M1 macrophage polarization. Conclusion: The inhibition of Axl reduced macrophage polarization toward the M1 phenotype
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