ArticleJournal of neuroinflammation2024
Microglial Pdcd4 deficiency mitigates neuroinflammation-associated depression via facilitating Daxx mediated PPARγ/IL-10 signaling.
Article in Journal of neuroinflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- PDCD4: A Double-Edged Sword in Neurological Diseases.Molecular neurobiology · 2026Review
- Review
- Lipopolysaccharide Upregulates Neuroinflammation, Oxidative Stress Responses, and Peroxiredoxins in Depression Models.Brain and behavior · 2026Article
- Interaction Between Microglial Lipid Droplet Metabolism and Immune Polarisation After Stroke: Mechanisms and Therapeutic Prospects.Cellular and molecular neurobiology · 2025Review
- Spatial Transcriptomics Reveals Transcriptomic and Immune Microenvironment Reprogramming during Thyroid Carcinoma Dedifferentiation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The central role of microglia in major depressive disorder and its potential as a therapeutic target.Frontiers in behavioral neuroscience · 2025Review
- Transcutaneous auricular vagus nerve stimulation alleviates inflammation-induced depression by modulating peripheral-central inflammatory cytokines and the NF-κB pathway in rats.Frontiers in immunology · 2025Article
- Neuroinflammation and stress-induced pathophysiology in major depressive disorder: mechanisms and therapeutic implications.Frontiers in cellular neuroscience · 2025Review
- Article
- Paeonol alleviates ulcerative colitis by modulating PPAR-γ and nuclear factor-κB activation.Scientific reports · 2024Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
The dysregulation of pro- and anti-inflammatory processes in the brain has been linked to the pathogenesis of major depressive disorder (MDD), although the precise mechanisms remain unclear. In this study, we discovered that microglial conditional knockout of Pdcd4 conferred protection against LPS-induced hyperactivation of microglia and depressive-like behavior in mice. Mechanically, microglial Pdcd4 plays a role in promoting neuroinflammatory responses triggered by LPS by inhibiting Daxx-mediated PPARγ nucleus translocation, leading to the suppression of anti-inflammatory cytokine IL-10 expression. Finally, the antidepressant effect of microglial Pdcd4 knockout under LPS-challenged conditions was abolished by intracerebroventricular injection of the IL-10 neutralizing antibody IL-10Rα. Our study elucidates the distinct involvement of microglial Pdcd4 in neuroinflammation, suggesting its potential as a therapeutic target for neuroinflammation-related depression.
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Registered trials
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