ArticleMolecular neurobiology2024
Arginine Methylation of β-Catenin Induced by PRMT2 Aggravates LPS-Induced Cognitive Dysfunction and Depression-Like Behaviors by Promoting Ferroptosis.
Article in Molecular neurobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 18 citations in OpenAlex.
- N 6 -methyladenosine modification regulates cell death in cognitive impairment.Neural regeneration research · 2026Article
- From Iron to Depression: The Crosstalk Between the Periphery and Brain.Neuroscience bulletin · 2026Review
- Targeting ferroptosis as a novel strategy for depressive mental disorders.Psychopharmacology · 2026Review
- Lipopolysaccharide Upregulates Neuroinflammation, Oxidative Stress Responses, and Peroxiredoxins in Depression Models.Brain and behavior · 2026Article
- The Fractalkine (FKN/CX3CL1) Pathway in Depression: A Critical Review of Its Role in Neuroinflammation and Therapeutic Potential.Neuropsychiatric disease and treatment · 2026Review
- The vicious cycle of neuroinflammation and ferroptosis in depression: mechanisms and therapeutic targets.Frontiers in neuroscience · 2026Review
- 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
- The role of microglia in neurodegenerative diseases: from the perspective of ferroptosis.Acta pharmacologica Sinica · 2025Review
- Ferroptosis: a new target for depression prevention and treatment.Journal of neural transmission (Vienna, Austria : 1996) · 2025Review
- The Ferroptosis-Mitochondrial Axis in Depression: Unraveling the Feedforward Loop of Oxidative Stress, Metabolic Homeostasis Dysregulation, and Neuroinflammation.Antioxidants (Basel, Switzerland) · 2025Review
- Ghrelin Induces Ferroptosis Resistance and M2 Polarization of Microglia to Alleviate Neuroinflammation and Cognitive Impairment in Alzheimer's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Exploring Ferroptosis-Related Genes in Depression: Insights Into Molecular Mechanisms and Potential Therapies.International journal of general medicine · 2025Article
- Neuroinflammation and stress-induced pathophysiology in major depressive disorder: mechanisms and therapeutic implications.Frontiers in cellular neuroscience · 2025Review
- Ferroptosis, pathogenesis and therapy in AS co-depression disease.Frontiers in pharmacology · 2025Review
- Ferroptosis-associated signaling pathways and therapeutic approaches in depression.Frontiers in neuroscience · 2025Review
- Iron homeostasis and ferroptosis in human diseases: mechanisms and therapeutic prospects.Signal transduction and targeted therapy · 2024Review
- Overexpression of ATF4 Inhibits Ferroptosis to Alleviate Anxiety Disorders by Activating the TGF-β Signaling Pathway.Neuropsychiatric disease and treatment · 2024Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Depression is a prevalent and debilitating psychiatric disorder, imposing substantial societal and individual burdens. This study aims to investigate the involvement of ferroptosis and microglial polarization in the pathogenesis of depression, as well as the underlying mechanism. Increased protein arginine methyltransferase 2 (PRMT2) expression was observed in BV2 cells and the hippocampus following lipopolysaccharide (LPS) stimulation. Mechanistically, alkylation repair homolog protein 5 (ALKBH5)-mediated m6A modification enhanced the stability of PRMT2 mRNA. PRMT2 promoted arginine methylation of β-catenin and induced proteasomal degradation of β-catenin proteins, resulting in transcriptional inhibition of glutathione peroxidase 4 (GPX4). The upregulation of PRMT2 further accelerated microglia polarization by activating ferroptosis through the β-catenin-GPX4 axis. Depletion of PRMT2 improved LPS-induced depressive- and anxiety-like behaviors as well as cognitive impairment by inhibiting ferroptosis and M1 polarization of microglia. Our findings underscore the crucial involvement of the ALKBH5-PRMT2-β-catenin-GPX4 axis in ferroptosis and M1 polarization of microglia, thereby offering novel insights into the pathogenesis interventions for depression.
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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.