ArticleJournal of neuroinflammation2019
Apelin-13/APJ system attenuates early brain injury via suppression of endoplasmic reticulum stress-associated TXNIP/NLRP3 inflammasome activation and oxidative stress in a AMPK-dependent manner after subarachnoid hemorrhage in rats.
Article in Journal of neuroinflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 1 of them a synthesis that pooled it.
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Who cites it
91 citing papers in PubMed, 1 synthesis or guideline pooled it, 197 citations in OpenAlex.
- Mechanisms of memory impairment in animal models of nontraumatic intracranial hemorrhage: A systematic review of the literature.Brain hemorrhages · 2022Pooled it
- Anesthesia inhalation agent sevoflurane induces perioperative cognitive impairment: Apelin/early growth response 1 axis induces ferritinophagy and exacerbates ferroptosis.Medical gas research · 2027Article
- Exerkine-Mediated Regulation of the NLRP3 Inflammasome in Neuroprotection: Mechanistic Insights and the Role of Exercise.Molecular neurobiology · 2026Review
- AMPK-NLRP3 Inflammasome Crosstalk: Structural Insights, Molecular Mechanisms, and Therapeutic Implications for Inflammation and Neuroinflammation.Molecular neurobiology · 2026Review
- Loss of AMPK potentiates inflammation by activating the infammasome in a preclinical mouse model of TBI.NeuroImmune pharmacology and therapeutics · 2026Article
- Associations of FGF23 and Apelin-13 with osteoporosis and diabetic peripheral neuropathy in postmenopausal women with type 2 diabetes mellitus.Frontiers in medicine · 2026Article
- Piperine improves ischemic brain injury by promoting the regulation of the AMPK/PGC-1α pathway by Apelin 13.Frontiers in pharmacology · 2026Article
- Apelin-13 Attenuates Blood-Brain Barrier Dysfunction Following Intracerebral Hemorrhage via Targeting the Keap1/Nrf2 Signaling.CNS neuroscience & therapeutics · 2025Article
- Pioglitazone Modulates Microglia M1/M2 Polarization Through PPAR-γ Pathway and Exerts Neuroprotective Effects in Experimental Subarachnoid Hemorrhage.Molecular neurobiology · 2025Article
- Silencing APLNR enhances the radiosensitivity of prostate cancer by modulating the PI3K/AKT/mTOR signaling pathway.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Article
- Inhibition of GPR17/ID2 Axis Improve Remyelination and Cognitive Recovery after SAH by Mediating OPC Differentiation in Rat Model.Translational stroke research · 2025Article
- A New Perspective on the Prediction and Treatment of Stroke: The Role of Uric Acid.Neuroscience bulletin · 2025Review
- A reactive oxygen species-responsive hydrogel loaded with Apelin-13 promotes the repair of spinal cord injury by regulating macrophage M1/M2 polarization and neuroinflammation.Journal of nanobiotechnology · 2025Article
- Astragaloside IV improves the survival rates of retinal ganglion cells in traumatic optic neuropathy by regulating autophagy mediated by the AMPK-MTOR-ULK signaling pathway.Molecular vision · 2025Article
- G Protein-Coupled Receptor 30 Attenuates Neuronal Pyroptosis Induced by Subarachnoid Hemorrhage.Mediators of inflammation · 2025Article
- Thioredoxin-interacting protein (TXNIP) inhibition promotes retinal ganglion cell survival and facilitates M1-like microglial transformation via the PI3K/Akt pathway in glaucoma.Molecular medicine (Cambridge, Mass.) · 2024Article
- A soluble garlic polysaccharide supplement alleviates fatigue in mice.NPJ science of food · 2024Article
- Promise of mesenchymal stem cell-derived extracellular vesicles for alleviating subarachnoid hemorrhage-induced brain dysfunction by neuroprotective and antiinflammatory effects.Brain, behavior, & immunity - health · 2024Review
- Protective effects of flavonoids against intracerebral and subarachnoid hemorrhage (Review).Experimental and therapeutic medicine · 2024Review
- Betulin ameliorates neuronal apoptosis and oxidative injury via DJ-1/Akt/Nrf2 signaling pathway after subarachnoid hemorrhage.CNS neuroscience & therapeutics · 2024Article
31 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundNeuroinflammation and oxidative stress play important roles in early brain injury following subarachnoid hemorrhage (SAH). This study is the first to show that activation of apelin receptor (APJ) by apelin-13 could reduce endoplasmic reticulum (ER)-stress-associated inflammation and oxidative stress after SAH.
methodsApelin-13, apelin siRNA, APJ siRNA, and adenosine monophosphate-activated protein kinase (AMPK) inhibitor-dorsomorphin were used to investigate if the activation of APJ could provide neuroprotective effects after SAH. Brain water content, neurological functions, blood-brain barrier (BBB) integrity, and inflammatory molecules were evaluated at 24 h after SAH. Western blotting and immunofluorescence staining were applied to assess the expression of target proteins.
resultsThe results showed that endogenous apelin, APJ, and p-AMPK levels were significantly increased and peaked in the brain 24 h after SAH. In addition, administration of exogenous apelin-13 significantly alleviated neurological functions, attenuated brain edema, preserved BBB integrity, and also improved long-term spatial learning and memory abilities after SAH. The underlying mechanism of the neuroprotective effects of apelin-13 is that it suppresses microglia activation, prevents ER stress from overactivation, and reduces the levels of thioredoxin-interacting protein (TXNIP), NOD-like receptor pyrin domain-containing 3 protein (NLRP3), Bip, cleaved caspase-1, IL-1β, TNFα, myeloperoxidase (MPO), and reactive oxygen species (ROS). Furthermore, the use of APJ siRNA and dorsomorphin abolished the neuroprotective effects of apelin-13 on neuroinflammation and oxidative stress.
conclusionsExogenous apelin-13 binding to APJ attenuates early brain injury by reducing ER stress-mediated oxidative stress and neuroinflammation, which is at least partly mediated by the AMPK/TXNIP/NLRP3 signaling pathway.
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