ArticleJournal of cellular and molecular medicine2021
SENP1 modulates microglia-mediated neuroinflammation toward intermittent hypoxia-induced cognitive decline through the de-SUMOylation of NEMO.
Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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18 citing papers in PubMed, 28 citations in OpenAlex.
- Intermittent Hypoxia Exacerbates Lipopolysaccharide-Induced Neurobehavioral Abnormalities: The Role of Neuroinflammation and Synaptic-Related Proteins.Brain and behavior · 2026Article
- Molecular and Cellular Signaling Pathways of the Effects of Hypoxia and Hypercapnia on the Mechanisms of Neuroinflammation.International journal of molecular sciences · 2026Review
- Differential cardiovascular and autonomic responses to structurally distinct intermittent hypoxia paradigms in rats.Hypertension research : official journal of the Japanese Society of Hypertension · 2026Article
- Death-associated protein kinase 1-dependent SENP1 degradation increases tau SUMOylation and leads to cognitive dysfunction in a mouse model for tauopathy.Molecular neurodegeneration · 2025Article
- Post-translational modifications regulating microglial inflammation in central nervous system disorders: a review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- SENP1: A perspective from immune cells to disease (Review).Oncology reports · 2025Review
- Polyamination with spermidine enhances pathogenic tau conformations while reducing filamentous aggregate formation in vitro.The Biochemical journal · 2025Article
- Chronic Intermittent Hypoxia-Induced Neural Injury: Pathophysiology, Neurodegenerative Implications, and Therapeutic Insights.CNS neuroscience & therapeutics · 2025Review
- Downregulation of Gbp2 Attenuates LPS-Induced Inflammation in BV2 Microglia Cells Through Inhibition of STAT1.Journal of inflammation research · 2025Article
- Regulation of the immune microenvironment by SUMO in diabetes mellitus.Frontiers in immunology · 2025Review
- Article
- Impact of Chronic Intermittent Hypoxia on Cognitive Function and Hippocampal Neurons in Mice: A Study of Inflammatory and Oxidative Stress Pathways.Nature and science of sleep · 2024Article
- Neuroprotective Effects of Moderate Hypoxia: A Systematic Review.Brain sciences · 2023Review
- Intermittent hypoxia treatments cause cellular priming in human microglia.Journal of cellular and molecular medicine · 2023Article
- Microglia dynamic response and phenotype heterogeneity in neural regeneration following hypoxic-ischemic brain injury.Frontiers in immunology · 2023Review
- The role of SUMOylation in the neurovascular dysfunction after acquired brain injury.Frontiers in pharmacology · 2023Review
- Overexpression of Foxc1 ameliorates sepsis‑associated encephalopathy by inhibiting microglial migration and neuroinflammation through the IκBα/NF‑κB pathway.Molecular medicine reports · 2022Article
- SENP1 modulates microglia-mediated neuroinflammation toward intermittent hypoxia-induced cognitive decline through the de-SUMOylation of NEMO.Journal of cellular and molecular medicine · 2021Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intermittent hypoxia (IH)-induced cognition decline is related to the neuroinflammation in microglia. SUMOylation is associated with multiple human diseases, which can be reversed by sentrin/SUMO-specific proteases 1 (SENP1). Herein, we investigated the role of SENP1 in IH-induced inflammation and cognition decline. BV-2 microglial cells and mice were used for inflammatory response and cognition function evaluation following IH treatment. Biochemical analysis and Morris water maze methods were used to elaborate the mechanism of SENP1 in IH impairment. Molecular results revealed that IH induced the inflammatory response, as evidenced by the up-regulation of NF-κB activation, IL-1β and TNF-α in vitro and in vivo. Moreover, IH decreased the expression of SENP1, and increased the SUMOylation of NEMO, not NF-κB P65. Moreover, SENP1 overexpression inhibited IH-induced inflammatory response and SUMOylation of NEMO. However, the inhibitions were abolished by siRNA-NEMO. In contrast, SENP1 depletion enhanced IH-induced inflammatory response and SUMOylation of NEMO, accompanying with increased latency and reduced dwell time in mice. Overall, the results demonstrated that SENP1 regulated IH-induced neuroinflammation by modulating the SUMOylation of NEMO, thus activating the NF-κB pathway, revealing that targeting SENP1 in microglia may represent a novel therapeutic strategy for IH-induced cognitive decline.
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