ArticleSignal transduction and targeted therapy2025
Astrocytic monoamine oxidase B (MAOB)-gamma-aminobutyric acid (GABA) axis as a molecular brake on repair following spinal cord injury.
Article in Signal transduction and targeted therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- TRANsCre-DIONE transdifferentiates scar-forming reactive astrocytes into functional motor neurons.Experimental & molecular medicine · 2026Article
- Article
- In-depth multimodal validation ofExperimental & molecular medicine · 2026Article
- Neurotransmitter Systems in Alzheimer's Disease.Current issues in molecular biology · 2026Review
- Beyond the Glial Scar: Fibroblasts as Dynamic Coordinators of Neuroprotection and Neuroinflammation Post-Brain Injury.Neuroscience bulletin · 2026Article
- USP44 Stabilizes MAOB via Deubiquitination to Inhibit Cisplatin Resistance in Lung Adenocarcinoma.International journal of genomics · 2026Article
- Astrocytic GABAergic signaling in perioperative neurocognitive disorders: mechanisms and intervention strategies.Frontiers in neuroscience · 2026Review
- Electroactive biomaterials modulating ion channels in nervous system regeneration.Regenerative biomaterials · 2026Review
- Astrocytic gamma-aminobutyric acid dysregulation as a therapeutic target for posttraumatic stress disorder.Signal transduction and targeted therapy · 2025Article
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Authors and funding
23 authors.
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Abstract
Neuroregeneration and remyelination rarely occur in the adult mammalian brain and spinal cord following central nervous system (CNS) injury. The glial scar has been proposed as a major contributor to this failure in the regenerative process. However, its underlying molecular and cellular mechanisms remain unclear. Here, we report that monoamine oxidase B (MAOB)-dependent excessive γ-aminobutyric acid (GABA) release from reactive astrocytes suppresses the CNS repair system by reducing brain‒derived neurotrophic factor (BDNF) and tropomyosin receptor kinase B (TrkB) expression in severe spinal cord injury (SCI) animal models. Genetic deletion of MAOB in a mouse SCI model promotes both functional and tissue recovery. Notably, the selective MAOB inhibitor, KDS2010, facilitates recovery and regeneration by disinhibiting the BDNF-TrkB axis in a rat SCI model. Its dose-dependent effects were further validated in a monkey SCI model. Moreover, KDS2010 demonstrated a tolerable safety profile and dose-proportional pharmacokinetics in healthy humans during a phase 1 clinical trial. This pathway therefore represents a pivotal target for overcoming the intrinsic barriers to CNS repair after injury. Our findings identify the astrocytic MAOB‒GABA axis as a crucial molecular and cellular brake on the CNS repair system following SCI and highlight the translational potential of KDS2010 as a promising therapeutic candidate for SCI treatment.
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