ArticleMolecular pain
Bortezomib-induced aerobic glycolysis contributes to chemotherapy-induced painful peripheral neuropathy.
Article in Molecular pain. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 47 citations in OpenAlex.
- Transcript architecture predetermines m6A remodeling and sensory neuron vulnerability in chemotherapy-induced peripheral neuropathy.bioRxiv : the preprint server for biology · 2026Article
- Neuronal metabolism role in ketogenic diet improvements in bortezomib-induced painful peripheral neuropathy mouse model.Pain reports · 2026Article
- The Crosstalk Between Brain Energy Metabolism and Neuropathic Pain: Mechanisms and Therapeutic Implications.Metabolites · 2025Review
- Absence of the axon initial segment in sensory neuron enhances resistance to amyotrophic lateral sclerosis.Brain : a journal of neurology · 2025Article
- Modulation of pain by ketones: a mini-review.American journal of physiology. Cell physiology · 2025Review
- Mitochondrial AThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Intrathecal Fumagillin Alleviates Chronic Neuropathy-Induced Nociceptive Sensitization and Modulates Spinal Astrocyte-Neuronal Glycolytic and Angiogenic Proteins.Molecular neurobiology · 2025Article
- Bortezomib-induced peripheral neuropathy: from molecular mechanisms to clinical management.Frontiers in pharmacology · 2025Review
- Discovery of Glucose Metabolism-Associated Genes in Neuropathic Pain: Insights from Bioinformatics.International journal of molecular sciences · 2024Article
- Intrathecal lactate dehydrogenase A inhibitors FX11 and oxamate alleviate chronic constriction injury-induced nociceptive sensitization through neuroinflammation and angiogenesis.The journal of headache and pain · 2024Article
- Glutamine Oxidation in Mouse Dorsal Root Ganglia Regulates Pain Resolution and Chronification.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- The Multifaceted Role of Alpha-Lipoic Acid in Cancer Prevention, Occurrence, and Treatment.Antioxidants (Basel, Switzerland) · 2024Review
- Article
- The ER membrane protein complex restricts mitophagy by controlling BNIP3 turnover.The EMBO journal · 2024Article
- Targeting metabolic pathways alleviates bortezomib-induced neuropathic pain without compromising anticancer efficacy in a sex-specific manner.Frontiers in pain research (Lausanne, Switzerland) · 2024Article
- Boron-Containing Compounds for Prevention, Diagnosis, and Treatment of Human Metabolic Disorders.Biological trace element research · 2023Review
- The ER membrane protein complex governs lysosomal turnover of a mitochondrial tail-anchored protein, BNIP3, to restrict mitophagy.bioRxiv : the preprint server for biology · 2023Article
- Tumor-secreted lactate contributes to an immunosuppressive microenvironment and affects CD8 T-cell infiltration in glioblastoma.Frontiers in immunology · 2023Article
- Recent advances in the treatment and prevention of peripheral neuropathy after multiple myeloma treatment.Ibrain · 2023Review
- Alpha-Lipoic Acid as an Antioxidant Strategy for Managing Neuropathic Pain.Antioxidants (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chemotherapy-induced painful peripheral neuropathy (CIPN) is the most common toxicity associated with widely used chemotherapeutics. CIPN is the major cause of dose reduction or discontinuation of otherwise life-saving treatment. Unfortunately, CIPN can persist in cancer survivors, which adversely affects their quality of life. Moreover, available treatments are vastly inadequate, warranting a better understanding of the biochemical and metabolic mechanisms that occur in response to chemotherapeutics which would be critical for the development of novel therapies for CIPN. Using extracellular flux analysis, this study demonstrated that the proteasome inhibitor, bortezomib, enhanced glycolysis while suppressing oxidative phosphorylation in the sensory neurons of mice. This metabolic phenotype is known as aerobic glycolysis. Bortezomib upregulated lactate dehydrogenase A and pyruvate dehydrogenase kinase 1, which consequently enhanced the production of lactate and repressed pyruvate oxidation, respectively. Moreover, lactate dehydrogenase A- and pyruvate dehydrogenase kinase 1-driven aerobic glycolysis was associated with increased extracellular acidification, augmented calcium responses, and pain in bortezomib-induced CIPN. Remarkably, pharmacological blockade and in vivo knockdown of lactate dehydrogenase A or pyruvate dehydrogenase kinase 1 reversed the metabolic phenotype, attenuated calcium responses, and alleviated pain induced by bortezomib. Collectively, these results elucidate the mechanisms by which bortezomib induces aerobic glycolysis. Moreover, these findings establish aerobic glycolysis as a metabolic phenotype that underpins bortezomib-induced CIPN.
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