ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
GFRα1 Promotes Axon Regeneration after Peripheral Nerve Injury by Functioning as a Ligand.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Biomaterial-assisted neuralization strategies for tissue engineering applications.Materials today. Bio · 2026Review
- Enhanced therapeutic potential of paeoniflorin and vitamin B12 in intracerebropeduncle ethidium bromide-induced multiple sclerosis-like pathology.Frontiers in pharmacology · 2026Article
- SYK regulates Schwann cell metabolic reprogramming to promote axonal regeneration in immune-mediated neuropathy.Journal of neuroinflammation · 2025Article
- Hydrogen sulfide protects against spinal cord pyroptosis via persulfidation of Rac1 after lumbosacral plexus nerve injury.Cell death discovery · 2025Article
- GFRα1 Promotes Axon Regeneration after Peripheral Nerve Injury by Functioning as a Ligand.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Extracellular Vesicles in Peripheral Nerve Regeneration: From Biology to Therapeutic Engineering.International journal of nanomedicine · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
The neurotrophic factor, Glial cell line derived neurotrophi factor (GDNF), exerts a variety of biological effects through binding to its receptors, GDNF family receptor alpha-1 (GFRα1), and RET. However, the existence of cells expressing GFRα1 but not RET raises the possibility that GFRα1 can function independently from RET. Here, it is shown that GFRα1 released from repair Schwann cells (RSCs) functions as a ligand in a GDNF-RET-independent manner to promote axon regeneration after peripheral nerve injury (PNI). Local administration of GFRα1 into injured nerve promoted axon regeneration, even more when combined with GDNF blockade. GFRα1 bound to a receptor complex consisting of NCAM and integrin α7β1 of dorsal root ganglion neurons in a GDNF-RET independent manner. This is further confirmed by the Ret Y1062F knock-in mice, which cannot transmit most of GDNF-RET signaling. Finally, local administration of GFRα1 into injured sciatic nerve promoted functional recovery. These findings reveal a novel role of GFRα1 as a ligand, the molecular mechanism supporting axon regeneration by RSCs, and a novel therapy for peripheral nerve repair.
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Registered trials
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