ReviewFrontiers in molecular neuroscience2022
NLRP3 Inflammasome Activation: A Therapeutic Target for Cerebral Ischemia-Reperfusion Injury.
Review in Frontiers in molecular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.
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Who cites it
67 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.
- Research progress on microglial pyroptosis and inflammasomes: a comprehensive analysis.Frontiers in aging neuroscience · 2025Pooled it
- Molecular mechanism of hydromorphone preconditioning in cerebral ischemia/reperfusion‑induced inflammatory injury.International journal of molecular medicine · 2026Article
- Blockade of the SP/NK1 receptor axis: multimodal neuroprotection via inflammatory suppression, hypoxic modulation, and lympho-vascular remodeling in global cerebral ischemia.Metabolic brain disease · 2026Article
- Activation of sarco/endoplasmic reticulum Ca²⁺-ATPase 2 (SERCA2) reduces brain injury and improves cognitive function following ischemic stroke.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026Article
- The Anti-Inflammatory Effect of Yangyin Tongnao Granule on Cerebral Ischemia-Reperfusion Injury in Rats.CNS neuroscience & therapeutics · 2026Article
- Pyroptosis in cerebral ischemia‑reperfusion injury: Molecular mechanisms and therapeutic implications (Review).Molecular medicine reports · 2026Review
- Umbilical cord mesenchymal stromal cells-derived HGF inhibits STING-mediated pyroptosis to alleviate cerebral ischemia/reperfusion injury via c-Met/β-catenin/RNF5 pathway.Journal of translational medicine · 2026Article
- Targeting PKC/NF-κB/NLRP3-driven NcRNA neuroinflammatory crosstalk by condensed tannins in global cerebral ischemia.Inflammopharmacology · 2026Review
- Mitochondria as a therapeutic target in neurodegeneration caused by hypoxia and ischemia during the perinatal period.Pharmacological reports : PR · 2026Review
- HIF-1α/BNIP3-mediated mitophagy mitigates cerebral ischemia/reperfusion injury in rats by suppressing NLRP3 inflammasome activation.European journal of medical research · 2026Article
- Recent advances in research on novel therapeutic mechanisms and strategies for exosome-based treatment of ischemic stroke.Frontiers in pharmacology · 2026Review
- Exercise-induced myokine irisin protects against obesity-associated ischemic stroke via integrin αVβ5 signaling.Frontiers in pharmacology · 2026Article
- Traditional Chinese medicine interventions targeting Wnt/β-catenin signaling in cerebral ischemia/reperfusion injury: a review.Frontiers in pharmacology · 2026Review
- Ozone protects against ischemia-reperfusion injury: molecular mechanisms.Frontiers in pharmacology · 2026Review
- Multi-target neuroprotective mechanisms of epigallocatechin-3-gallate (EGCG) in stroke: from molecular pathways to nanomedicine delivery and clinical translation.Frontiers in pharmacology · 2026Review
- TAT and RVG Co-modified MSC-derived Exosomes-mediated Delivery of microRNA-15b-5p Inhibitor Alleviate Cerebral Ischemia and Reperfusion-induced Neuronal Apoptosis by Promoting HTR2C-ERK Signaling.Molecular neurobiology · 2025Article
- Anti-inflammatory Effects of Membrane Vesicles from Eubacterium rectale via the NLRP3 Signal Pathway.Probiotics and antimicrobial proteins · 2025Article
- Gallic Acid Alleviates Cerebral Ischemia-reperfusion Injury in Mice by Mediating Microglial Polarization Through the NLRP3/mTOR Axis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Targeting the NLRP3 inflammasome with natural products for ischemia-reperfusion injury across organs: mechanisms, structure-activity relationships, and delivery innovations.Inflammopharmacology · 2025Review
- Immunological Mechanisms and Therapeutic Strategies in Cerebral Ischemia-Reperfusion Injury: From Inflammatory Response to Neurorepair.International journal of molecular sciences · 2025Review
7 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Millions of patients are suffering from ischemic stroke, it is urgent to figure out the pathogenesis of cerebral ischemia-reperfusion (I/R) injury in order to find an effective cure. After I/R injury, pro-inflammatory cytokines especially interleukin-1β (IL-1β) upregulates in ischemic brain cells, such as microglia and neuron. To ameliorate the inflammation after cerebral I/R injury, nucleotide-binding oligomerization domain (NOD), leucine-rich repeat (LRR), and pyrin domain-containing protein 3 (NLRP3) inflammasome is well-investigated. NLRP3 inflammasomes are complicated protein complexes that are activated by endogenous and exogenous danger signals to participate in the inflammatory response. The assembly and activation of the NLRP3 inflammasome lead to the caspase-1-dependent release of pro-inflammatory cytokines, such as interleukin (IL)-1β and IL-18. Furthermore, pyroptosis is a pro-inflammatory cell death that occurs in a dependent manner on NLRP3 inflammasomes after cerebral I/R injury. In this review, we summarized the assembly and activation of NLRP3 inflammasome; moreover, we also concluded the pivotal role of NLRP3 inflammasome and inhibitors, targeting the NLRP3 inflammasome in cerebral I/R injury.
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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.