ArticleFrontiers in immunology2024
Ischemia-induced endogenous Nrf2/HO-1 axis activation modulates microglial polarization and restrains ischemic brain injury.
Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Human Dental Pulp Stem Cell Secretome Restores Ischemic Stroke-Impaired Motor and Cognitive Functions by Reprogramming Redox and Inflammatory Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Evaluation of the Nrf2-Keap1 Pathway in Patients with Acute Cerebral Ischemic Disease.Medicina (Kaunas, Lithuania) · 2026Article
- The Role of Nuclear Factor Erythroid 2-Related Factor 2 in the Crosstalk Between Oxidative Stress and M1/M2 Microglial Polarization Following Ischemic Stroke.Molecular neurobiology · 2026Review
- Puerarin attenuates myocardial ischemia‑reperfusion injury by inhibiting myocardium pyroptosis via the NRF2/HO‑1 signaling pathway.Molecular medicine reports · 2026Article
- Changes in NR2ab Antibody Levels in the Blood of Patients Depending on their Condition: Acute or Chronic Cerebral Ischaemia.Acta medica Lituanica · 2026Article
- Tracing Inflammation in Ischemic Stroke: Biomarkers and Clinical Insight.International journal of molecular sciences · 2025Review
- Association between oxidative balance score with cardiovascular - kidney - metabolic syndrome and all-cause mortality among US population.Frontiers in nutrition · 2025Article
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Authors and funding
6 authors.
Funding
Abstract
Cerebral ischemic stroke accounts for more than 80% of all stroke cases. During cerebral ischemia, reactive oxygen species produced in the ischemic brain induce oxidative stress and inflammatory responses. Nrf2 is a transcription factor responsible for regulating cellular redox balance through the induction of protective antioxidant and phase II detoxification responses. Although the induction of endogenous Nrf2/HO-1 axis activation has been observed in the ischemic brain, whether ischemia-induced endogenous Nrf2/HO-1 axis activation plays a role in modulating microglia (MG) phenotypes and restraining ischemic brain injury is not characterized and requires further exploration. To investigate that, we generated mice with Nrf2 knockdown specifically in MG to rigorously assess the role of endogenous Nrf2 activation in ischemic brain injury after stroke. Our results showed that MG-specific Nrf2 knockdown exacerbated ischemic brain injury after stroke. We found that Nrf2 knockdown altered MG phenotypes after stroke, in which increased frequency of inflammatory MG and decreased frequency of anti-inflammatory MG were detected in the ischemic brain. Moreover, we identified attenuated Nrf2/HO-1 axis activation led to increased CD68/IL-1β and suppressed CD206 expression in MG, resulting in aggravated inflammatory MG in MG-specific Nrf2 knockdown mice after stroke. Intriguingly, using type II diabetic preclinical models, we revealed that diabetic mice exhibited attenuated Nrf2/HO-1 axis activation in MG and exacerbated ischemic brain injury after stroke that phenocopy mice with MG-specific Nrf2 knockdown. Finally, the induction of exogenous Nrf2/HO-1 axis activation in MG through pharmacological approaches ameliorated ischemic brain injury in diabetic mice. In conclusion, our findings provide cellular and molecular insights demonstrating ischemia-induced endogenous Nrf2/HO-1 axis activation modulates MG phenotypes and restrains ischemic brain injury. These results further strengthen the therapeutic potential of targeting Nrf2/HO-1 axis in MG for the treatment of ischemic stroke and diabetic stroke.
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