ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Schwann cell mitochondrial metabolism supports long-term axonal survival and peripheral nerve function.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers.
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Who cites it
100 citing papers in PubMed, 209 citations in OpenAlex.
- Molecular Mediators Associated With Myelination, Demyelination, and Remyelination in the Peripheral Nervous System.Journal of the peripheral nervous system : JPNS · 2026Review
- Review
- A Generalized Deep Learning Pipeline for Stain-Invariant Ultrastructural Segmentation in Peripheral Nerves.Journal of imaging · 2026Article
- NR4A3 alleviates diabetic neuropathy via GLS2-mediated mitochondrial repair and Schwann cell differentiation.iScience · 2026Article
- Mitochondrial dysfunction at the intersection of alcohol use disorder and chronic pain.Function (Oxford, England) · 2026Review
- Prostaglandin D2 Synthase Controls Schwann Cells Metabolism and Peripheral Myelin Homeostasis.Glia · 2026Article
- Integrating pharmacovigilance signals with real-world validation: a study on neurological events associated with PCSK9 inhibitors.Frontiers in medicine · 2026Article
- Schwann cell Lrp1 deletion drives trigeminal neuron sensitization and orofacial pain by modulating mitochondrial function and TRPV1/TRPA1 activity.The journal of headache and pain · 2025Article
- Review
- Article
- PMP2 Enhances Schwann Cell Metabolism and Promotes Myelination.Journal of neurochemistry · 2025Article
- Review
- Imeglimin improves hyperglycemia and hypoglycemia-induced cell death and mitochondrial dysfunction in immortalized adult mouse Schwann IMS32 cells.Journal of diabetes investigation · 2025Article
- Engineering the Future of Restorative Clinical Peripheral Nerve Surgery.Advanced healthcare materials · 2025Review
- The low-density lipoprotein receptor-related protein-1 (LRP1) in Schwann cells controls mitochondria homeostasis in peripheral nerves.Progress in neurobiology · 2025Article
- Strengthening monocarboxylate transporters by adiponectin receptor agonist ameliorates diabetic peripheral neuropathy.Cell communication and signaling : CCS · 2025Article
- 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
- NMDA Receptors Coordinate Metabolic Reprogramming and Mitophagy in Schwann Cells to Promote Peripheral Nerve Regeneration.Research (Washington, D.C.) · 2025Article
- Schwann Cells and Their Exosomes: Research Progress and Prospect in Spinal Cord Injury.Neural plasticity · 2025Review
40 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Mitochondrial dysfunction is a common cause of peripheral neuropathies. While the role of neuron and axonal mitochondria in peripheral nerve disease is well appreciated, whether Schwann cell (SC) mitochondrial deficits contribute to peripheral neuropathies is unclear. Here, we examine how SC mitochondrial dysfunction affects axonal survival and contributes to the decline of peripheral nerve function by generating mice with SC-specific mitochondrial deficits. These mice (Tfam-SCKOs) were produced through the tissue-specific deletion of the mitochondrial transcription factor A gene (Tfam), which is essential for mitochondrial DNA (mtDNA) transcription and maintenance. Tfam-SCKOs were viable, but as they aged, they developed a progressive peripheral neuropathy characterized by nerve conduction abnormalities as well as extensive muscle denervation. Morphological examination of Tfam-SCKO nerves revealed early preferential loss of small unmyelinated fibers followed by prominent demyelination and degeneration of larger-caliber axons. Tfam-SCKOs displayed sensory and motor deficits consistent with this pathology. Remarkably, the severe mtDNA depletion and respiratory chain abnormalities in Tfam-SCKO mice did not affect SC proliferation or survival. Mitochondrial function in SCs is therefore essential for maintenance of axonal survival and normal peripheral nerve function, suggesting that SC mitochondrial dysfunction contributes to human peripheral neuropathies.
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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.