ArticleExperimental & molecular medicine2025
Dysregulation of FGFR1 signaling in the hippocampus facilitates depressive disorder.
Article in Experimental & molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Signaling Connectomics: A Brain-wide Framework for Intercellular Communication.Experimental neurobiology · 2026Article
- HIF1α Attenuated the Lung Ischemia-Reperfusion Injury by Activating the miR-485/Notch1 Signalling.Journal of cellular and molecular medicine · 2026Article
- AI-driven decoding of naturalistic behaviors enables tailored detection of depressive-like behavior in mice.Nature communications · 2025Article
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Authors and funding
8 authors.
Funding
Abstract
Major depressive disorder (MDD) is a complex psychological disorder with a sophisticated molecular etiology. Although its connection with fibroblast growth factor receptor 1 (FGFR1) in the hippocampus is known, the precise mechanisms underlying its pathophysiology remain unclear. Here we conduct a comprehensive analysis of the molecular profile of the hippocampus in patients with MDD. We identified a distinct overexpression of FGFR1 specifically within the dentate gyrus of patients with MDD. Through the use of optogenetic techniques for the in vivo spatiotemporal dissection of FGFR1 signaling, we uncovered a sequential FGFR1-Notch-brain-derived neurotrophic factor (BDNF) pathway within the dentate gyrus, which can ultimately induce adult hippocampal neurogenesis, significantly contributing to antidepressant effects. We discovered that the dysregulation of this axis by the protein Numb, which demonstrates an age-related increase in individuals with MDD, is closely associated with the development of depressive phenotypes. Remarkably, targeting Numb to restore this axis effectively reversed the depressive phenotype, thus offering new insights into potential therapeutic strategies.
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Registered trials
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