ArticleNature neuroscience2014
Metabolic regulator LKB1 is crucial for Schwann cell-mediated axon maintenance.
Article in Nature neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers.
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Who cites it
122 citing papers in PubMed, 207 citations in OpenAlex.
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- A Novel Central-Peripheral Interface: The Auditory Nerve Glial Transition Zone Exhibits Enhanced Age-Related Immune and Glial Cell Dysfunction.bioRxiv : the preprint server for biology · 2026Article
- Clemastine Restores Myelination Protein Expression in S16 Schwann Cells by Enhancing AMPK Activation and Reducing HBiomolecules & therapeutics · 2026Article
- Prostaglandin D2 Synthase Controls Schwann Cells Metabolism and Peripheral Myelin Homeostasis.Glia · 2026Article
- Testing an inverse link between limbic alpha-synucleinopathy and myelin markers in mice and humans.NPJ Parkinson's disease · 2026Article
- The role of secretome from mesenchymal stromal cells in promoting nerve regeneration after neurotmesis.Stem cell research & therapy · 2026Article
- The auditory nerve glial transition zone is a focal site of age-related immune-myelin interactions.Frontiers in immunology · 2026Article
- Dysregulated lactate metabolism synergizes with ALS genetic risk factors to accelerate motor decline.PloS one · 2026Article
- SYK regulates Schwann cell metabolic reprogramming to promote axonal regeneration in immune-mediated neuropathy.Journal of neuroinflammation · 2025Article
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- Dysregulated lactate metabolism synergizes with ALS genetic risk factors to accelerate motor decline.bioRxiv : the preprint server for biology · 2025Article
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- PCSK9 deficiency promotes the development of peripheral neuropathy.JCI insight · 2025Article
- Pmp2+ Schwann Cells Maintain the Survival of Large-Caliber Motor Axons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Schwann Cell-Specific Ablation of Beclin 1 Impairs Myelination and Leads to Motor and Sensory Neuropathy in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Qizhi Kebitong Formula Ameliorates Sciatic Nerve Injury in Streptozocin-induced Diabetic Mice through PERK/ATF4/CHOP Endoplasmic Reticulum Stress Signaling Pathway.Current pharmaceutical design · 2025Article
- Pharmacologically targeting Schwann cells to improve regeneration following nerve damage.Frontiers in cell and developmental biology · 2025Review
- Morphometric characteristics of tibial nerve and their relationship with age.Brain communications · 2025Article
62 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 1 country.
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Abstract
Schwann cells (SCs) promote axonal integrity independently of myelination by poorly understood mechanisms. Current models suggest that SC metabolism is critical for this support function and that SC metabolic deficits may lead to axonal demise. The LKB1-AMP-activated protein kinase (AMPK) kinase pathway targets several downstream effectors, including mammalian target of rapamycin (mTOR), and is a key metabolic regulator implicated in metabolic diseases. We found through molecular, structural and behavioral characterization of SC-specific mutant mice that LKB1 activity is central to axon stability, whereas AMPK and mTOR in SCs are largely dispensable. The degeneration of axons in LKB1 mutants was most dramatic in unmyelinated small sensory fibers, whereas motor axons were comparatively spared. LKB1 deletion in SCs led to abnormalities in nerve energy and lipid homeostasis and to increased lactate release. The latter acts in a compensatory manner to support distressed axons. LKB1 signaling is essential for SC-mediated axon support, a function that may be dysregulated in diabetic neuropathy.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.