ArticleOxidative medicine and cellular longevity2021
iTRAQ-Based Quantitative Proteomics Indicated Nrf2/OPTN-Mediated Mitophagy Inhibits NLRP3 Inflammasome Activation after Intracerebral Hemorrhage.
Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 36 citations in OpenAlex.
- Inhibiting NLRP3 Inflammasome Activation to Alleviate Retinal Inflammation and Protect the Optic Nerve of OPTN(E50K)Mice.Inflammation · 2025Article
- Carotid Endarterectomy Ameliorates Cognitive Impairment in Clinical and Experimental Unilateral Carotid Artery Stenosis.Journal of the American Heart Association · 2025Article
- Targeting the Interplay Between Autophagy and the Nrf2 Pathway in Parkinson's Disease with Potential Therapeutic Implications.Biomolecules · 2025Review
- A new perspective on the regulation of neuroinflammation in intracerebral hemorrhage: mechanisms of NLRP3 inflammasome activation and therapeutic strategies.Frontiers in immunology · 2025Review
- Mitochondrial quality control and transfer communication in neurological disorders and neuroinflammation.Frontiers in immunology · 2025Review
- Article
- Signature and function of plasma exosome-derived circular RNAs in patients with hypertensive intracerebral hemorrhage.Molecular genetics and genomics : MGG · 2024Article
- Mitochondrial stress: a key role of neuroinflammation in stroke.Journal of neuroinflammation · 2024Review
- Mitophagy in intracerebral hemorrhage: a new target for therapeutic intervention.Neural regeneration research · 2024Review
- Review
- Mechanism and treatment of intracerebral hemorrhage focus on mitochondrial permeability transition pore.Frontiers in molecular neuroscience · 2024Review
- Mitophagy-associated programmed neuronal death and neuroinflammation.Frontiers in immunology · 2024Review
- Intracerebral Hemorrhage-Induced Brain Injury: the Role of Lysosomal-Associated Transmembrane Protein 5.Molecular neurobiology · 2023Article
- Emerging trends and hotspots of Nuclear factor erythroid 2-related factor 2 in nervous system diseases.World journal of clinical cases · 2023Article
- Review
- Interplay between Gut Microbiota and NLRP3 Inflammasome in Intracerebral Hemorrhage.Nutrients · 2022Review
- Perspectives on the mechanism of pyroptosis after intracerebral hemorrhage.Frontiers in immunology · 2022Review
- Erythrophagocytosis by Microglia/Macrophage in Intracerebral Hemorrhage: From Mechanisms to Translation.Frontiers in cellular neuroscience · 2022Review
- The Novel Nrf2 Activator Omaveloxolone Regulates Microglia Phenotype and Ameliorates Secondary Brain Injury after Intracerebral Hemorrhage in Mice.Oxidative medicine and cellular longevity · 2022Article
- Autophagy regulates inflammation in intracerebral hemorrhage: Enemy or friend?Frontiers in cellular neuroscience · 2022Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intracerebral hemorrhage- (ICH-) induced secondary brain injury (SBI) is a very complex pathophysiological process. However, the molecular mechanisms and drug targets of SBI are highly intricate and still elusive, yet a clear understanding is crucial for the treatment of SBI. In the current study, we aimed to confirm that nuclear factor-E2-related factor 2 (Nrf2)/Optineurin- (OPTN-) mediated mitophagy alleviated SBI by inhibiting nucleotide-binding oligomerization domain-like receptor pyrin domain-containing 3 (NLRP3) inflammasome activation based on the isobaric tag for relative and absolute quantization (iTRAQ) quantification proteomics. Human ICH brain specimens were collected for iTRAQ-based proteomics analysis. Male Nrf2 wild-type (WT) and knockout (KO) mice were employed to establish ICH murine models. The survival rate, hematoma volume, neurofunctional outcomes, blood-brain barrier (BBB) permeability, brain edema, spatial neuronal death, NLRP3 inflammasome, inflammatory response, mitochondrial function, and mitophagy level were evaluated after ICH. The iTRAQ quantification analysis showed that the differentially expressed proteins (DEPs), Nrf2 and NLRP3, were closely associated with the initiation and development of SBI after ICH. The Nrf2 KO mice had a significantly lower survival rate, bigger hematoma volume, worse neurological deficits, and increased BBB disruption, brain edema, and neuronal death when compared with the Nrf2 WT mice after ICH. Furthermore, Nrf2 KO enhanced NLRP3 inflammasome activation and neuroinflammation as evidenced by the NF-
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