ArticleActa pharmacologica Sinica2025
Tofacitinib prevents depressive-like behaviors through decreased hippocampal microgliosis and increased BDNF levels in both LPS-induced and CSDS-induced mice.
Article in Acta pharmacologica Sinica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Article
- Hippocampal REDD1 inhibition is critical for alleviating depressive-like behaviors.Acta pharmacologica Sinica · 2026Article
- Clinical advances and multifactorial pathophysiological mechanisms of neuropsychiatric comorbidity in systemic sclerosis.Frontiers in immunology · 2026Review
- What to do when the first TNF inhibitor fails in rheumatoid arthritis: stratified expert recommendations from a scoping review and Delphi consensus.Therapeutic advances in musculoskeletal disease · 2026Article
- JAK/STAT signaling pathway inhibitors in neurodegenerative diseases: current status and future perspectives.Frontiers in aging neuroscience · 2026Review
- Lipopolysaccharide induced mouse depression model can better simulate changes in peripheral blood FFAs in alMDD.PloS one · 2026Article
- NADPH alleviates LPS-induced neuropathology and depression-like behaviors by suppressing microglial inflammatory response.Translational psychiatry · 2025Article
- Mechanism of Microbiota-Gut-Brain in Perimenopausal Depression: An Inflammatory Perspective.Expert reviews in molecular medicine · 2025Review
- Neuronal CCL2 responds to hyperglycaemia and contributes to anxiety disorders in the context of diabetes.Nature metabolism · 2025Article
- Evolving Landscape of HER2-Targeted Therapies for Gastric Cancer Patients.Current treatment options in oncology · 2025Review
- Salvianolic acid B alleviates depression-like behaviors by reducing neuronal injury and promoting neurogenesis in a manner associated with JAK-STAT signaling pathway inhibition.Frontiers in neurologyArticle
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Authors and funding
15 authors.
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Abstract
Depressive disorders are a global mental health challenge that is closely linked to inflammation, especially in the post-COVID-19 era. The JAK-STAT pathway, which is primarily associated with inflammatory responses, is not fully characterized in the context of depressive disorders. Recently, a phase 3 retrospective cohort analysis heightened that the marketed JAK inhibitor tofacitinib is beyond immune diseases and has potential for preventing mood disorders. Inspired by these clinical facts, we investigated the role of the JAK-STAT signaling pathway in depression and comprehensively assessed the antidepressant effect of tofacitinib. We found that aberrant activation of the JAK-STAT pathway is highly conserved in the hippocampus of classical depressive mouse models: LPS-induced and chronic social defeat stress (CSDS)-induced depressive mice. Mechanistically, the JAK-STAT pathway mediates proinflammatory cytokine production and microgliosis, leading to synaptic defects in the hippocampus of both depressive models. Remarkably, the JAK inhibitor tofacitinib effectively reverses these phenomena, contributing to its antidepressant effect. These findings indicate that the JAK/STAT pathway could be implicated in depressive disorders, and suggest that the JAK inhibitor tofacitinib has a potential translational implication for preventing mood disorders far beyond its current indications.
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