ArticleJournal of neuroinflammation2018
Aggf1 attenuates neuroinflammation and BBB disruption via PI3K/Akt/NF-κB pathway after subarachnoid hemorrhage in rats.
Article in Journal of neuroinflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 2 of them syntheses that pooled it.
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Who cites it
90 citing papers in PubMed, 2 syntheses or guidelines pooled it, 155 citations in OpenAlex.
- Effects of Dl-3-n-butylphthalide on neurological function, hemodynamics and Hcy concentration in cerebral hemorrhage: a systematic review and meta-analysis.Frontiers in pharmacology · 2024Pooled it
- The Role of MicroRNAs in Predicting the Neurological Outcome of Patients with Subarachnoid Hemorrhage: A Meta-analysis.Cellular and molecular neurobiology · 2023Pooled it
- PDCD1 Signaling in Microglia Can Reduce Neuroinflammation and Apoptosis Induced by Traumatic Brain Injury by Regulating PI3K/Akt Signaling Pathway, Thereby Alleviating Neurological Dysfunction.Molecular neurobiology · 2026Article
- AGGF1 delays endothelial cellular senescence through the TGFB3-TAK1-AMPK signaling axis.Biogerontology · 2026Article
- Empagliflozin-pretreated mesenchymal stem cell-derived extracellular vesicles facilitate cardiac repair via AGGF1.Journal of nanobiotechnology · 2026Article
- Cardiomyocyte-Derived Apelin Rescues Viral Myocarditis-Induced Cardiac Lymphatic Dysfunction and Remodeling.JACC. Basic to translational science · 2026Article
- S100A8 aggravates sepsis-associated encephalopathy by promoting PFKFB3-dependent glycolysis and microglial neuroinflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- The PI3K-AKT-VEGF Signaling Pathway Contributes to Doxorubicin-induced Chemotherapy-related Cognitive Impairment.Current neuropharmacology · 2026Article
- Epidermal growth factor receptor modulation for neural repair: Implications for neurodegenerative disease therapy.Frontiers in molecular neuroscience · 2026Review
- Astragaloside IV suppresses neuroinflammation via PI3K/Akt/NF-κB to ameliorate cerebral ischemia-reperfusion injury based on network pharmacology analysis and experimental validation.Frontiers in immunology · 2026Article
- AGGF1-primed endothelial progenitor cells alleviate ischaemia-reperfusion injury in diabetic hearts.Scientific reports · 2025Article
- Inhibition of GPR17/ID2 Axis Improve Remyelination and Cognitive Recovery after SAH by Mediating OPC Differentiation in Rat Model.Translational stroke research · 2025Article
- Agathis dammara Extract and its Monomer Araucarone Attenuate Abdominal Aortic Aneurysm in Mice.Cardiovascular drugs and therapy · 2025Article
- Inhibition of USP30 Promotes Mitophagy by Regulating Ubiquitination of MFN2 by Parkin to Attenuate Early Brain Injury After SAH.Translational stroke 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
- 6-Hydroxygenistein Ameliorates High Altitude Brain Injury via Activating PI3K/AKT Signaling Pathway Based on Transcriptomic Analysis and Experimental Validation.Drug design, development and therapy · 2025Article
- Dynamic mechanisms and targeted interventions in cerebral ischemia-reperfusion injury: pathological cascade from ischemia to reperfusion and promising therapeutic strategies.Frontiers in neuroscience · 2025Review
- Astrocyte-microglia crosstalk in subarachnoid hemorrhage: mechanisms and treatments.Frontiers in immunology · 2025Review
- Targeting PI3K/Akt in Cerebral Ischemia Reperfusion Injury Alleviation: From Signaling Networks to Targeted Therapy.Molecular neurobiology · 2024Review
- Article
30 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundNeuroinflammation and blood-brain barrier (BBB) disruption are two critical mechanisms of subarachnoid hemorrhage (SAH)-induced brain injury, which are closely related to patient prognosis. Recently, angiogenic factor with G-patch and FHA domain 1 (Aggf1) was shown to inhibit inflammatory effect and preserve vascular integrity in non-nervous system diseases. This study aimed to determine whether Aggf1 could attenuate neuroinflammation and preserve BBB integrity after experimental SAH, as well as the underlying mechanisms of its protective roles.
methodsTwo hundred forty-nine male Sprague-Dawley rats were subjected to the endovascular perforation model of SAH. Recombinant human Aggf1 (rh-Aggf1) was administered intravenously via tail vein injection at 1 h after SAH induction. To investigate the underlying neuroprotection mechanism, Aggf1 small interfering RNA (Aggf1 siRNA) and PI3K-specific inhibitor LY294002 were administered through intracerebroventricular (i.c.v.) before SAH induction. SAH grade, neurological score, brain water content, BBB permeability, Western blot, and immunohistochemistry were performed.
resultsExpression of endogenous Aggf1 was markedly increased after SAH. Aggf1 was primarily expressed in endothelial cells and astrocytes, as well as microglia after SAH. Administration of rh-Aggf1 significantly reduced brain water content and BBB permeability, decreased the numbers of infiltrating neutrophils, and activated microglia in the ipsilateral cerebral cortex following SAH. Furthermore, rh-Aggf1 treatment improved both short- and long-term neurological functions after SAH. Meanwhile, exogenous rh-Aggf1 significantly increased the expression of PI3K, p-Akt, VE-cadherin, Occludin, and Claudin-5, as well as decreased the expression of p-NF-κB p65, albumin, myeloperoxidase (MPO), TNF-α, and IL-1β. Conversely, knockdown of endogenous Aggf1 aggravated BBB breakdown, inflammatory response and neurological impairments at 24 h after SAH. Additionally, the protective roles of rh-Aggf1 were abolished by LY294002.
conclusionsTaken together, exogenous Aggf1 treatment attenuated neuroinflammation and BBB disruption, improved neurological deficits after SAH in rats, at least in part through the PI3K/Akt/NF-κB pathway.
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