ArticleJournal of cellular and molecular medicine2022
Immunoproteasome modulates NLRP3 inflammasome-mediated neuroinflammation under cerebral ischaemia and reperfusion conditions.
Article in Journal of cellular and molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 24 citations in OpenAlex.
- The immunoproteasome as a neuroimmune hub in the central nervous system: from proteostasis stress to inflammatory pathology.Journal of neuroinflammation · 2026Review
- Review
- Inflammasomes in Cardiovascular Diseases: Current Knowledge and Future Perspectives.International journal of molecular sciences · 2025Review
- Acupuncture alleviates hemorrhagic transformation after delayed rt-PA treatment for acute ischemic stroke by regulating the mitophagy-NLRP3 inflammasome pathway.Frontiers in neurology · 2025Article
- NLRP3 Inflammasome Triggers Inflammation of Obstructive Sleep Apnea.Current molecular medicine · 2025Review
- Tetrahydrocurcumin Protects Microglial Cells AgainstInternational journal of medical sciences · 2025Article
- Biological and therapeutic significance of targeting NLRP3 inflammasome in the brain and the current efforts to develop brain-penetrant inhibitors.Advances in pharmacology (San Diego, Calif.) · 2025Review
- Cpeb4-mediated Dclk2 promotes neuronal pyroptosis induced by chronic cerebral ischemia through phosphorylation of Ehf.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Article
- A Combination of Astragaloside IV and Hydroxysafflor Yellow A Attenuates Cerebral Ischemia-Reperfusion Injury via NF-κB/NLRP3/Caspase-1/GSDMD Pathway.Brain sciences · 2024Article
- Targeting Microglial Immunoproteasome: A Novel Approach in Neuroinflammatory-Related Disorders.ACS chemical neuroscience · 2024Review
- Hypoxic Preconditioning Attenuates Neuroinflammation via Inhibiting NF-κB/NLRP3 Axis Mediated by p-MLKL after Transient Global Cerebral Ischemia.Molecular neurobiology · 2024Article
- Immunoproteasome Subunit Low Molecular Mass Peptide 2 (LMP2) Deficiency Ameliorates LPS/AβMolecular neurobiology · 2024Article
- MCC950 Regulates Stem Cells Destiny Through Modulating SIRT3-NLRP3 Inflammasome Dynamics During Oxygen Glucose Deprivation.Stem cell reviews and reports · 2023Article
- Inhibitors of the NLRP3 inflammasome pathway as promising therapeutic candidates for inflammatory diseases (Review).International journal of molecular medicine · 2023Review
- Signaling pathways involved in ischemic stroke: molecular mechanisms and therapeutic interventions.Signal transduction and targeted therapy · 2022Review
- Immunoproteasome modulates NLRP3 inflammasome-mediated neuroinflammation under cerebral ischaemia and reperfusion conditions.Journal of cellular and molecular medicine · 2022Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Compelling evidence showed that both nucleotide-binding oligomerization domain-like receptor family, pyrin domain-containing protein 3 (NLRP3) inflammasomes and the immunoproteasome participate in neuroinflammatory responses in cerebral ischaemia injury. Moreover, inhibition of either NLRP3 inflammasomes or the immunoproteasome attenuates both neuroinflammation and neurological deterioration during ischaemic stroke. However, the underlying mechanism between the immunoproteasome and NLRP3 inflammasomes under ischaemic stroke conditions remains to be established. In this study, using both in vitro and in vivo ischaemic models, we demonstrated that the immunoproteasome inhibition reduced the expressions of NLRP3 inflammasome-associated proteins, including NLRP3, apoptosis-associated speck-like protein (ASC), caspase-1 and mature cytokines (interleukin [IL]-1β and IL-18). It also downregulated the levels of nuclear factor (NF)-κB and pyroptotic- and apoptotic-related proteins, and improved cell viability. In addition, inhibition of NF-κB by the small molecule inhibitor Bay-11-7082 led to lower levels of NLRP3 inflammasomes and cleaved caspase-1 proteins in BV2 cells after oxygen-glucose deprivation and reoxygenation. Together, these findings suggest that the immunoproteasome may be responsible for inducing the expression and activation of NLRP3 inflammasomes via the NF-κB pathway. Therapeutic interventions that target activation of the immunoproteasome/NF-κB/NLRP3 inflammasome pathway may provide novel prospects for the future treatment of ischaemic stroke.
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