ArticleAging2021
Depletion of SENP1-mediated PPARγ SUMOylation exaggerates intermittent hypoxia-induced cognitive decline by aggravating microglia-mediated neuroinflammation.
Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- Molecular Drivers of Cognitive Decline and Neuroprotection in Obstructive Sleep Apnea: A Narrative Review.Antioxidants (Basel, Switzerland) · 2026Review
- Intelligent nanoliposome ameliorate chronic intermittent hypoxia-mediated neuronal injury via a dual regulation microglial inflammation strategy.Materials today. Bio · 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
- Programmed cell death in the cognitive impairment of obstructive sleep apnea.Cell & bioscience · 2025Review
- Impact of hypoxia on the hippocampus: A review.Medicine · 2025Review
- The role of microRNAs in pathophysiology and diagnostics of metabolic complications in obstructive sleep apnea patients.Frontiers in molecular neuroscience · 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-Mediated deSUMOylation Regulates the Tumor Remodeling of Glioma Stem Cells Under Hypoxic Stress.Technology in cancer research & treatmentArticle
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intermittent hypoxia (IH)-associated cognition decline is related to the neuroinflammation of microglia. SUMOylation is a post-translational modification related to multiple human diseases, which can be reversed by SENP1. Studies showed that SENP1 and PPARγ play essential roles in restricting inflammation by blocking NF-κB activation. However, the mechanism remains unclear. Herein, we investigated the precise mechanism underlying SENP1 and PPARγ in cognitive decline after IH insult. Biochemical analysis results revealed that IH triggered the inflammatory response and neuronal apoptosis, increased the SUMOylation of PPARγ, and decreased the level of PPARγ compared to that in the normoxia group. After SENP1 downregulation, the inflammatory response, neuronal apoptosis and the SUMOylation of PPARγ were enhanced, and the level of PPARγ was further decreased
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Registered trials
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.