ArticleCNS neuroscience & therapeutics2022
Pharmacological inhibition of epidermal growth factor receptor attenuates intracranial aneurysm formation by modulating the phenotype of vascular smooth muscle cells.
Article in CNS neuroscience & therapeutics, 2022. 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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14 citing papers in PubMed, 20 citations in OpenAlex.
- XIAP down-regulation inhibits RIPK2 ubiquitination-mediated insulin resistance.Endocrine connections · 2026Article
- Macrophage migration inhibitory factor-CD74 axis drives vascular smooth muscle cell-induced M1 macrophage polarization to exacerbate intracranial aneurysm inflammation.Frontiers in immunology · 2025Article
- Experimental and clinical tests of FDA-approved kinase inhibitors for the treatment of neurological disorders (update 2024).Exploration of drug science · 2025Article
- Effects of KLF11 on Vascular Smooth Muscle Cells and its Underlying Mechanisms in Intracranial Aneurysm.Biochemical genetics · 2024Article
- Pharmaceutical Modulation of Intracranial Aneurysm Development and Rupture.Journal of clinical medicine · 2024Review
- Evaluation of the EMBOPIPE flow diverter device: in vivo and in vitro experiments.Chinese neurosurgical journal · 2024Article
- WNTA5-mediated miR-374a-5p regulates vascular smooth muscle cell phenotype transformation and M1 macrophage polarization impacting intracranial aneurysm progression.Scientific reports · 2024Article
- Interstitial Fluid Shear Stress Induces the Synthetic Phenotype Switching of VSMCs to Release Pro-calcified Extracellular Vesicles via EGFR-MAPK-KLF5 Pathway.International journal of biological sciences · 2024Article
- Receptor Tyrosine Kinase: Still an Interesting Target to Inhibit the Proliferation of Vascular Smooth Muscle Cells.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2023Review
- FDA-Approved Kinase Inhibitors in Preclinical and Clinical Trials for Neurological Disorders.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Identifying and validating key genes mediating intracranial aneurysm rupture using weighted correlation network analysis and exploration of personalized treatment.Annals of translational medicine · 2022Article
- Hsa_circ_0031608: A Potential Modulator of VSMC Phenotype in the Rupture of Intracranial Aneurysms.Frontiers in molecular neuroscience · 2022Article
- Pharmacological inhibition of epidermal growth factor receptor attenuates intracranial aneurysm formation by modulating the phenotype of vascular smooth muscle cells.CNS neuroscience & therapeutics · 2022Article
- PRMT5 inhibition suppresses the PI3K/AKT pathway to attenuate vascular smooth muscle cell pathological phenotype in intracranial aneurysm.Frontiers in neurologyArticle
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo study the effect of pharmacological inhibition of epidermal growth factor receptor (EGFR) on intracranial aneurysm (IA) initiation.
methodsHuman IA samples were analyzed for the expression of p-EGFR and alpha smooth muscle actin (α-SMA) by immunofluorescence (IF). Rat models of IA were established to evaluate the ability of the EGFR inhibitor, erlotinib, to attenuate the incidence of IA. We analyzed anterior cerebral artery tissues by pathological and proteomic detection for the expression of p-EGFR and relevant proteins, and vessel casting was used to evaluate the incidence of aneurysms in each group. Rat vascular smooth muscle cells (VSMCs) and endothelial cells were extracted and used to establish an in vitro co-culture model in a flow chamber with or without erlotinib treatment. We determined p-EGFR and relevant protein expression in VSMCs by immunoblotting analysis.
resultsEpidermal growth factor receptor activation was found in human IA vessel walls and rat anterior cerebral artery walls. Treatment with erlotinib markedly attenuated the incidence of IA by inhibiting vascular remodeling and pro-inflammatory transformation of VSMC in rat IA vessel walls. Activation of EGFR in rat VSMCs and phenotypic modulation of rat VSMCs were correlated with the strength of shear stress in vitro, and treatment with erlotinib reduced phenotypic modulation of rat VSMCs. In vitro experiments also revealed that EGFR activation could be induced by TNF-α in human brain VSMCs.
conclusionsThese results suggest that EGFR plays a critical role in the initiation of IA and that the EGFR inhibitor erlotinib protects rats from IA initiation by regulating phenotypic modulation of VSMCs.
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