ArticleChinese medical journal2025
Paroxetine alleviates dendritic cell and T lymphocyte activation via GRK2-mediated PI3K-AKT signaling in rheumatoid arthritis.
Article in Chinese medical journal, 2025. 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.
- Efficacy of Paroxetine as an Adjuvant Therapy in Rheumatoid Arthritis Patients: A Randomized Controlled Study.Drug design, development and therapy · 2025Trial
- Recent advances in the development of GRK2 inhibitors: blocking the interaction of GRK2 with its partners.Acta pharmacologica Sinica · 2026Review
- Regulation of G protein-coupled receptor kinase 2 and its role in tumors.Journal of translational medicine · 2026Review
- Therapeutic effects of Melittin acupoint injection on rheumatoid arthritis through autophagy activation and PI3K/AKT/mTOR pathway inhibition.Quantitative imaging in medicine and surgery · 2026Article
- Total Glucosides of Paeony Alleviates Acute Kidney Injury by Inhibiting Dendritic Cells and T-Cell Communication.Advances in pharmacological and pharmaceutical sciences · 2026Article
- Paroxetine suppresses 27-hydroxycholesterol-induced responses in THP-1 human monocytic cells by regulating the AKT/mTORC1 pathway.Scientific reports · 2025Article
- From metabolic dysregulation to neurodegenerative pathology: the role of hyperglycemia, oxidative stress, and blood-brain barrier breakdown in T2D-driven Alzheimer's disease.Metabolic brain disease · 2025Review
- CD8Frontiers in immunology · 2025Article
- Shared immunological pathways in rheumatoid arthritis-related interstitial lung disease.Frontiers in immunology · 2025Review
- The role of SOX18 in nasopharyngeal carcinoma: implications for prognosis and therapy.American journal of translational research · 2025Article
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Abstract
backgroundG protein-coupled receptor kinase 2 (GRK2) could participate in the regulation of diverse cells via interacting with non-G-protein-coupled receptors. In the present work, we explored how paroxetine, a GRK2 inhibitor, modulates the differentiation and activation of immune cells in rheumatoid arthritis (RA).
methodsThe blood samples of healthy individuals and RA patients were collected between July 2021 and March 2022 from the First Affiliated Hospital of Anhui Medical University. C57BL/6 mice were used to induce the collagen-induced arthritis (CIA) model. Flow cytometry analysis was used to characterize the differentiation and function of dendritic cells (DCs)/T cells. Co-immunoprecipitation was used to explore the specific molecular mechanism.
resultsIn patients with RA, high expression of GRK2 in peripheral blood lymphocytes, accompanied by the increases of phosphatidylinositol 3 kinase (PI3K), protein kinase B (AKT), and mammalian target of rapamycin (mTOR). In animal model, a decrease in regulatory T cells (T regs ), an increase in the cluster of differentiation 8 positive (CD8 + ) T cells, and maturation of DCs were observed. Paroxetine, when used in vitro and in CIA mice, restrained the maturation of DCs and the differentiation of CD8 + T cells, and induced the proportion of T regs . Paroxetine inhibited the secretion of pro-inflammatory cytokines, the expression of C-C motif chemokine receptor 7 in DCs and T cells. Simultaneously, paroxetine upregulated the expression of programmed death ligand 1, and anti-inflammatory cytokines. Additionally, paroxetine inhibited the PI3K-AKT-mTOR metabolic pathway in both DCs and T cells. This was associated with a reduction in mitochondrial membrane potential and changes in the utilization of glucose and lipids, particularly in DCs. Paroxetine reversed PI3K-AKT pathway activation induced by 740 Y-P (a PI3K agonist) through inhibiting the interaction between GRK2 and PI3K in DCs and T cells.
conclusionParoxetine exerts an immunosuppressive effect by targeting GRK2, which subsequently inhibits the metabolism-related PI3K-AKT-mTOR pathway of DCs and T cells in RA.
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