ArticleFrontiers in cellular neuroscience2021
The Role of NF-κB Triggered Inflammation in Cerebral Ischemia.
Article in Frontiers in cellular neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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Who cites it
37 citing papers in PubMed, 57 citations in OpenAlex.
- Taraxerol Alleviates Cerebral Ischemia-Reperfusion Induced Inflammation and Ferroptosis via Regulating AKT/NF-κB Pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- TNFα-induced endothelial extracellular vesicles regulate astrocyte function: an integrated transcriptomic and proteomic study.Fluids and barriers of the CNS · 2026Article
- Temporal Vulnerability of the Blood-Brain Interface in Stroke: Molecular Mechanisms of Circadian Dynamics, Inflammation, and Aging.International journal of molecular sciences · 2026Review
- Astrocyte-derived IL-17A facilitates angiogenesis following ischemia-like injury via an IL-6-dependent STAT3-VEGF signaling cascade.Behavioral and brain functions : BBF · 2026Article
- Therapeutic Potential of PCSK9 Inhibitors in Regulating Neuroinflammation in Acute Ischemic Stroke.CNS drugs · 2026Review
- Subchronic low-dose tributyltin exposure is associated with parallel hypothalamic IL-10 suppression and ovarian inflammatory-endocrine alterations in female rats.Scientific reports · 2026Article
- Integrated multi-omics identifies macrophage ARG1-mediated deacetylation with causal and diagnostic implications in ischemic stroke.iScience · 2026Article
- Targeting PKC/NF-κB/NLRP3-driven NcRNA neuroinflammatory crosstalk by condensed tannins in global cerebral ischemia.Inflammopharmacology · 2026Review
- Neuroprotective Mechanisms of Hyperbaric Oxygen Therapy in Cerebral Ischemia-Hypoxia Injury Following Cardiopulmonary Resuscitation.International journal of medical sciences · 2026Review
- The Nodding syndrome cerebrospinal fluid proteome: a lens into neurodevelopmental failure consistent with environmentally triggeredFrontiers in molecular neuroscience · 2026Article
- Advances in the mechanisms of electroacupuncture in the treatment of cerebral ischemia-reperfusion injury.Frontiers in neuroscience · 2026Review
- Exploring Therapeutic and Multitarget Mechanism of Molsidomine on Cerebral Ischemia: Molecular Docking and Multifaceted In Silico Study.Advances in experimental medicine and biology · 2026Article
- HDAC1 dysregulation promotes pro-inflammatory microglial activation and aggravates post-stroke neuroinflammation.Annals of medicine · 2025Article
- Blocking S1PJournal of advanced research · 2025Article
- Modulatory Potential of Alpinetin on Inflammation, Oxidative Stress, Apoptosis, and Mitochondrial Dynamics in a Rat Middle Cerebral Artery Occlusion Model of Ischemic Stroke.International journal of molecular sciences · 2025Article
- NXC736, a Functional Antagonist of S1PMolecules (Basel, Switzerland) · 2025Article
- Cardiovascular Risk Factors Involved in Hemorrhagic Transformation After Intravenous Thrombolytic Therapy in Patients with Acute Ischemic Stroke.International journal of molecular sciences · 2025Review
- Progesterone Receptor Agonist, Nestorone, Exerts Long-Term Neuroprotective Effects Against Permanent Focal Cerebral Ischemia in Adult and Aged Male Rats.Translational stroke research · 2025Article
- Association of blood biomarkers for neural injury with recent, frequent exposure to partnered sexual strangulation in young adult women.The journal of sexual medicine · 2025Article
- The Ambiguous Role of HMGB1 Across the Hallmarks of Aging: A Narrative Review.Clinical interventions in aging · 2025Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Cerebral ischemia is a devastating disease that affects many people worldwide every year. The neurodegenerative damage as a consequence of oxygen and energy deprivation, to date, has no known effective treatment. The ischemic insult is followed by an inflammatory response that involves a complex interaction between inflammatory cells and molecules which play a role in the progression towards cell death. However, there is presently a matter of controversy over whether inflammation could either be involved in brain damage or be a necessary part of brain repair. The inflammatory response is triggered by inflammasomes, key multiprotein complexes that promote secretion of pro-inflammatory cytokines. An early event in post-ischemic brain tissue is the release of certain molecules and reactive oxygen species (ROS) from injured neurons which induce the expression of the nuclear factor-kappaB (NF-κB), a transcription factor involved in the activation of the inflammasome. There are conflicting observations related to the role of NF-κB. While some observe that NF-κB plays a damaging role, others suggest it to be neuroprotective in the context of cerebral ischemia, indicating the need for additional investigation. Here we discuss the dual role of the major inflammatory signaling pathways and provide a review of the latest research aiming to clarify the relationship between NF-κB mediated inflammation and neuronal death in cerebral ischemia.
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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.