ArticleEuropean journal of medical research2024
Circulating inflammatory biomarkers and risk of intracranial aneurysm: a Mendelian randomization study.
Article in European journal of medical research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 2 of them syntheses that pooled it.
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Who cites it
12 citing papers in PubMed, 2 syntheses or guidelines pooled it, 14 citations in OpenAlex.
- Mendelian randomization studies on cardiometabolic factors and intracranial aneurysms: A systematic literature analysis.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025Pooled it
- Vascular Endothelial Growth Factor and the Pathogenesis of Intracranial Aneurysms: A Systematic Review on the Missing Link in a Complex Pathway.Journal of the American Heart Association · 2024Pooled it
- Article
- Subarachnoid hemorrhage: epidemiology, risk factors, pathogenesis, and clinical therapies.Molecular biomedicine · 2026Review
- Multiomics genetic insights into potential molecular targets for intracranial aneurysm.Stroke and vascular neurology · 2026Article
- Interpretable Machine Learning Identifies Key Inflammatory and Morphological Drivers of Intracranial Aneurysm Rupture Risk.Bioengineering (Basel, Switzerland) · 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
- Bi-directional effects between inflammatory molecules and intracranial aneurysm.Neurosurgical review · 2024Article
- Predictive value of the systemic immune-inflammation index for periprocedural complications in flow diverter treatment for patients with intracranial aneurysms.Neurosurgical review · 2024Article
- Causal effects of inflammatory cytokines on cardiovascular diseases: Insights from genetic evidence.Heliyon · 2024Article
- Endothelial Progenitor Cells: A Review of Molecular Mechanisms in the Pathogenesis and Endovascular Treatment of Intracranial Aneurysms.Neuromolecular medicine · 2024Review
- Exploring causal correlations of inflammatory biomarkers in idiopathic normal-pressure hydrocephalus: insights from bidirectional Mendelian randomization analysis.Frontiers in aging neuroscience · 2024Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundIntracranial aneurysm (IA) accounts for a substantial source of non-traumatic subarachnoid hemorrhage, with inflammation postulated as a potential factor in its pathogenesis. The present study aims at evaluating the association between circulating inflammatory cytokines and risk of IA under a bidirectional two-sample Mendelian randomization (MR) design.
methodsFor primary analysis, summary statistics of inflammatory regulators was obtained from a genome-wide association study (GWAS) comprising 8293 Finnish participants. Summary data of IA were extracted from a GWAS which comprised 7495 cases and 71,934 controls in European descent. For targeted analysis, summary statistics were extracted from two proteomic studies, which recruit 3301 and 5368 European participants, respectively. Summary data of IA were acquired from FinnGen study with 5342 cases and 342,673 controls. We employed inverse variance weighted (IVW) method as main approach, with sensitivity analyses using weighted median, MR-Egger, and MR-PRESSO methods. Reverse MR analyses were conducted to minimize bias from reverse causality.
resultsNo causation of cytokines with IA subtypes was identified in both primary and targeted analysis after Bonferroni correction. In primary analysis, vascular endothelial growth factor (VEGF) and fibroblast growth factor basic (bFGF) levels were suggestively associated with aneurysmal subarachnoid hemorrhage (aSAH) [VEGF → aSAH: OR = 1.15, 95%CI 1.04-1.26, P = 0.005; bFGF → aSAH: OR = 0.62, 95% CI 0.42-0.92, P = 0.02]. Statistical significance failed to replicate in targeted analysis. Instead, suggestive protective effects for aSAH were identified in FGF-9 (FGF-9 → aSAH: OR = 0.74, 95% CI 0.62-0.89, P = 0.001) and FGF-16 (FGF-16 → aSAH: OR = 0.84, 95% CI 0.72-0.97, P = 0.017). Furthermore, reverse analyses identified suggestive effect of unruptured IA on RANTES, MIF, GRO-alpha, FGF-16, and FGF-19. Result remained robust after applying sensitivity tests.
conclusionsNo causality of inflammatory biomarkers on the risk of IA subtypes was identified. Future large-scale studies are in need to evaluate the temporal dynamics of cytokines in conjunction with IA.
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