ArticleCell death & disease2023
Local production of reactive oxygen species drives vincristine-induced axon degeneration.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 24 citations in OpenAlex.
- Preclinical Pharmacokinetic and Pharmacological Profiling of B339, a Novel SARM1 Inhibitor for the Treatment of Vincristine-induced Peripheral Neuropathy.Pharmaceutical research · 2026Article
- MZT2A drives epithelial-mesenchymal transition in lung adenocarcinoma via the LGALS3BP/ITGB1/TGF-β/smad2 axis.iScience · 2026Article
- Article
- Peripheral Nerve Surgery and Chemotherapy: A Review, Index, and Decision Tree for Nerve Surgeons Considering Neurotization After Oncological Nerve Injuries.Neurosurgery practice · 2026Review
- Molecular and Mechanistic Divergence of Seizures in Pediatric Acute Lymphoblastic Leukemia: CNS Infiltration Versus Chemotherapy-Induced Neurotoxicity.International journal of molecular sciences · 2026Review
- Mechanistic insights and therapeutic interventions of mitochondrial quality control in chemotherapy-related cognitive impairment.Neoplasia (New York, N.Y.) · 2026Review
- Axonopathy: mechanisms and potential therapeutic targets for neurodegenerative diseases.Translational neurodegeneration · 2026Review
- Clinical outcomes of adding vincristine to procarbazine-lomustine in patients with gliomas: insights from current evidence.Ecancermedicalscience · 2026Article
- Pharmacogenomics of treatment toxicities in pediatric B-Cell ALL: toward safer precision therapy.Frontiers in pharmacology · 2026Review
- Programmed axon degeneration: mechanism, inhibition and therapeutic potential.Nature reviews. Neuroscience · 2026Review
- Mechanisms and treatment of cancer therapy-induced peripheral and central neurotoxicity.Nature reviews. Cancer · 2025Review
- Attenuating Neurotoxicity Through Fecal Microbiota Transplant: Mechanisms and Therapeutic Potential.Molecular neurobiology · 2025Review
- Chronic Oxaliplatin Treatment Induces CIPN in Mice via Activation of the TXNIP Pathway.Molecular neurobiology · 2025Article
- Article
- Article
- PDH Inhibition inBiomedicines · 2025Article
- Review
- DLK-dependent axonal mitochondrial fission drives degeneration after axotomy.Nature communications · 2024Article
- Molsidomine provides neuroprotection against vincristine-induced peripheral neurotoxicity through soluble guanylyl cyclase activation.Scientific reports · 2024Article
- Augustus Waller's foresight realized: SARM1 in peripheral neuropathies.Current opinion in neurobiology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Neurological side effects arising from chemotherapy, such as severe pain and cognitive impairment, are a major concern for cancer patients. These major side effects can lead to reduction or termination of chemotherapy medication in patients, negatively impacting their prognoses. With cancer survival rates improving dramatically, addressing side effects of cancer treatment has become pressing. Here, we use iPSC-derived human neurons to investigate the molecular mechanisms that lead to neurotoxicity induced by vincristine, a common chemotherapeutic used to treat solid tumors. Our results uncover a novel mechanism by which vincristine causes a local increase in mitochondrial proteins that produce reactive oxygen species (ROS) in the axon. Vincristine triggers a cascade of axon pathology, causing mitochondrial dysfunction that leads to elevated axonal ROS levels and SARM1-dependent axon degeneration. Importantly, we show that the neurotoxic effect of increased axonal ROS can be mitigated by the small molecule mitochondrial division inhibitor 1 (mdivi-1) and antioxidants glutathione and mitoquinone, identifying a novel therapeutic avenue to treat the neurological effects of chemotherapy.
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What OpenQuestion holds
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.