ArticleMolecular pain2015
Mitochondrial and bioenergetic dysfunction in trauma-induced painful peripheral neuropathy.
Article in Molecular pain, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.
- Association of Genetic Variant at Chromosome 12q23.1 With Neuropathic Pain Susceptibility.JAMA network open · 2021Pooled it
- Peripheral nerve injury alters metabolic function and neuronal excitability through the Lin28/let-7 pathway.Science advances · 2026Article
- Wavelength dependent effects of red and infrared photobiomodulation on neuropathic pain, skeletal muscle integrity, and mitochondrial respiration.Lasers in medical science · 2026Article
- Mitochondrial Dysfunction and Endoplasmic Reticulum Stress in Chronic Pain.Brain sciences · 2026Review
- Targeting Supramolecular Active Complexes of NaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- High-resolution metabolic profiling of the effects of early-life stress after peripheral nerve injury.The journal of pain · 2026Article
- Single-cell and experimental analyses identify mitochondria-related genes Hmgcs2, Nudt5, and Cpt1c in painful diabetic peripheral neuropathy.Scientific reports · 2026Article
- Article
- Mitochondrial dysfunction at the intersection of alcohol use disorder and chronic pain.Function (Oxford, England) · 2026Review
- A novel extracellular flux assay workflow uncovers impaired sciatic nerve mitochondrial respiration in diabetic db/db mice.Cell communication and signaling : CCS · 2026Article
- Unveiling the Role of CCL3: A Driver of CIPN in Colon Cancer Patients?Biomedicines · 2025Review
- Mitochondrial Gene Regulation and Pain Susceptibility: A Multi-Omics Causal Inference Study.International journal of molecular sciences · 2025Article
- Review
- Lactate alleviates trigeminal neuralgia symptoms in mice by suppressing neuroinflammation.The Journal of international medical research · 2025Article
- The Burning Pain Transcriptome in the Mouse Primary Somatosensory Cortex.International journal of molecular sciences · 2025Article
- The Integrated Transcriptome Bioinformatics Analysis of Energy Metabolism-Related Profiles for Dorsal Root Ganglion of Neuropathic Pain.Molecular neurobiology · 2025Article
- Role of Mitochondrial Dysfunction in Neuropathy.International journal of molecular sciences · 2025Review
- Clinical measures in chronic neuropathic pain are related to the Kennedy and endocannabinoid pathways.European journal of clinical investigation · 2025Article
- Intrathecal Fumagillin Alleviates Chronic Neuropathy-Induced Nociceptive Sensitization and Modulates Spinal Astrocyte-Neuronal Glycolytic and Angiogenic Proteins.Molecular neurobiology · 2025Article
- Plant food-derived antioxidant nutrients in neuroprotection against chemotherapy-induced neurotoxicity: from molecular mechanisms to clinical applications.Frontiers in nutrition · 2025Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundMitochondrial dysfunction is observed in various neuropathic pain phenotypes, such as chemotherapy induced neuropathy, diabetic neuropathy, HIV-associated neuropathy, and in Charcot-Marie-Tooth neuropathy. To investigate whether mitochondrial dysfunction is present in trauma-induced painful mononeuropathy, a time-course of mitochondrial function and bioenergetics was characterized in the mouse partial sciatic nerve ligation model.
resultsTraumatic nerve injury induces increased metabolic indices of the nerve, resulting in increased oxygen consumption and increased glycolysis. Increased metabolic needs of the nerve are concomitant with bioenergetic and mitochondrial dysfunction. Mitochondrial dysfunction is characterized by reduced ATP synthase activity, reduced electron transport chain activity, and increased futile proton cycling. Bioenergetic dysfunction is characterized by reduced glycolytic reserve, reduced glycolytic capacity, and increased non-glycolytic acidification.
conclusionTraumatic peripheral nerve injury induces persistent mitochondrial and bioenergetic dysfunction which implies that pharmacological agents which seek to normalize mitochondrial and bioenergetic dysfunction could be expected to be beneficial for pain treatment. Increases in both glycolytic acidification and non-glycolytic acidification suggest that pH sensitive drugs which preferentially act on acidic tissue will have the ability to preferential act on injured nerves without affecting healthy tissues.
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Registered trials
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.