SynthesisInternational journal of molecular sciences2023
The Role of NF-κB in Intracranial Aneurysm Pathogenesis: A Systematic Review.
Synthesis in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 29 citations in OpenAlex.
- Endothelial dysfunction: A central mechanism linking autosomal dominant polycystic kidney disease and intracranial aneurysms (Review).International journal of molecular medicine · 2026Review
- Harnessing Regulatory T Cells to Modulate Acute Brain Injury: From Mechanisms to Therapy.Molecular neurobiology · 2026Review
- Cortical thinning and volumetric alterations in patients with unruptured intracranial aneurysms: insights from surface-based morphometry.Neurosurgical review · 2026Article
- Risk of Cardiovascular Disease Mortality in Patients With Diagnosed Cancer and Associated Genetic and Proteomic Mechanisms: A UK Biobank-Based Cohort Study.Journal of the American Heart Association · 2026Article
- Identification and validation of a pyroptosis-related gene signature in intracranial aneurysm.Open life sciences · 2026Article
- Identification of Key Genes and miRNA-mRNA Regulatory Networks Associated with Intracranial Aneurysm Progression by Integrative Bioinformatics Analysis.Current medicinal chemistry · 2026Article
- The quercetin-serotonin transporter (SERT) connection: a new hope for depression therapy?Psychopharmacology · 2026Review
- First Direct Evidence of Accelerated Molecular Aging in Intracranial Aneurysmal Tissue.Aging cell · 2025Article
- Molecular Targets for Intracranial Aneurysm Treatment.International journal of molecular sciences · 2025Review
- Platelet factor 4 and stromal cell-derived factor are novel prognostic biomarkers for cerebral vasospasm and mortality after subarachnoid hemorrhage.Scientific reports · 2025Article
- Mechanisms and interventions in aneurysmal subarachnoid hemorrhage: Unraveling the role of inflammatory responses and cell death in early brain injury (Review).Molecular medicine reports · 2025Review
- Identification of pivotal genes and regulatory networks associated with SAH based on multi-omics analysis and machine learning.Scientific reports · 2025Article
- 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
- Headache and Intracranial Aneurysm: A Bidirectional Mendelian Randomization Study.Current neurovascular research · 2025Article
- Mechanisms and potential therapeutic molecular targets in blood-brain barrier disruption following subarachnoid hemorrhage: a review of early brain injury.Frontiers in neurology · 2025Review
- The multifaceted roles and diagnostic-therapeutic potential of LINC01410 in malignant tumors and non-malignant disorders.Frontiers in immunology · 2025Review
- Article
- Mendelian randomization demonstrates a causal link between peripheral circulating acylcarnitines and intracranial aneurysms.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Article
- LINC01410 accelerates the invasion of trophoblast cells by modulating METTL3/Fas.Molecular biology reports · 2024Article
- Exploring the causal role of immune cells in cerebral aneurysm through single-cell transcriptomics and Mendelian randomization analysis.Clinical and experimental immunology · 2024Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intracranial aneurysms (IAs) are abnormal dilations of the cerebral vessels, which pose a persistent threat of cerebral hemorrhage. Inflammation is known to contribute to IA development. The nuclear factor "kappa-light-chain-enhancer" of activated B-cells (NF-κB) is the major driver of inflammation. It increases the expression of inflammatory markers and matrix metalloproteinases (MMPs), which contribute heavily to the pathogenesis of IAs. NF-κB activation has been linked to IA rupture and resulting subarachnoid hemorrhage. Moreover, NF-κB activation can result in endothelial dysfunction, smooth muscle cell phenotypic switching, and infiltration of inflammatory cells in the arterial wall, which subsequently leads to the initiation and progression of IAs and consequently results in rupture. After a systematic search, abstract screening, and full-text screening, 30 research articles were included in the review. In this systematic review, we summarized the scientific literature reporting findings on NF-κB's role in the pathogenesis of IAs. In conclusion, the activation of the NF-κB pathway was associated with IA formation, progression, and rupture.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.