ArticleMolecular and cellular neurosciences2018
Peroxisomes contribute to oxidative stress in neurons during doxorubicin-based chemotherapy.
Article in Molecular and cellular neurosciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 54 citations in OpenAlex.
- Attenuation of DOX-Associated Biochemical and Histological Brain Alterations.Veterinary medicine and science · 2026Article
- Caloric restriction reprograms skeletal muscle molecular pathways in non-human primates: potential relevance to human aging biology.Skeletal muscle · 2026Article
- Mechanistic insights and therapeutic interventions of mitochondrial quality control in chemotherapy-related cognitive impairment.Neoplasia (New York, N.Y.) · 2026Review
- Multimodal Cancer Therapy and Accelerated Brain Aging: Mechanisms, Biomarkers, and Clinical Consequences.Current oncology (Toronto, Ont.) · 2026Review
- Canadine protects against doxorubicin-induced cardiac and brain injury by inhibiting Oxidative stress.BMC pharmacology & toxicology · 2026Article
- Enhancing the Water Solubility and Efficacy of Anticancer Drugs Using Hydroxypropyl-β-Cyclodextrin.International journal of molecular sciences · 2026Review
- Pathological α-synuclein perturbs nuclear integrity.Neurobiology of disease · 2025Article
- Lycium barbarum Glycopeptide Alleviates Neomycin-Induced Ototoxicity by Inhibiting Tryptophan Hydroxylase-Mediated Serotonin Biosynthesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Different Mechanisms in Doxorubicin-Induced Neurotoxicity: Impact of BRCA Mutations.International journal of molecular sciences · 2025Review
- Pathological α-Synuclein Perturbs Nuclear Integrity.bioRxiv : the preprint server for biology · 2025Article
- Pexophagy and Oxidative Stress: Focus on Peroxisomal Proteins and Reactive Oxygen Species (ROS) Signaling Pathways.Antioxidants (Basel, Switzerland) · 2025Review
- Peroxisome and pexophagy in neurological diseases.Fundamental research · 2024Review
- Establishment of human pluripotent stem cell-derived cortical neurosphere model to study pathomechanisms and chemical toxicity in Kleefstra syndrome.Scientific reports · 2024Article
- [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Targeting therapy-induced senescence as a novel strategy to combat chemotherapy-induced peripheral neuropathy.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2024Review
- The Tardigrade damage suppressor protein Dsup promotes DNA damage in neurons.Molecular and cellular neurosciences · 2023Article
- Neurotoxic Effect of Doxorubicin Treatment on Cardiac Sympathetic Neurons.International journal of molecular sciences · 2022Article
- Genetically controlled mtDNA deletions prevent ROS damage by arresting oxidative phosphorylation.eLife · 2022Article
- Chemobrain in Breast Cancer: Mechanisms, Clinical Manifestations, and Potential Interventions.Drug safety · 2022Review
- Cognitive adverse effects of chemotherapy and immunotherapy: are interventions within reach?Nature reviews. Neurology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Doxorubicin, a commonly used anti-neoplastic agent, causes severe neurotoxicity. Doxorubicin promotes thinning of the brain cortex and accelerates brain aging, leading to cognitive impairment. Oxidative stress induced by doxorubicin contributes to cellular damage. In addition to mitochondria, peroxisomes also generate reactive oxygen species (ROS) and promote cell senescence. Here, we investigated if doxorubicin affects peroxisomal homeostasis in neurons. We demonstrate that the number of peroxisomes is increased in doxorubicin-treated neurons and in the brains of mice which underwent doxorubicin-based chemotherapy. Pexophagy, the specific autophagy of peroxisomes, is downregulated in neurons, and peroxisomes produce more ROS. 2-hydroxypropyl-β-cyclodextrin (HPβCD), an activator of the transcription factor TFEB, which regulates expression of genes involved in autophagy and lysosome function, mitigates damage of pexophagy and decreases ROS production induced by doxorubicin. We conclude that peroxisome-associated oxidative stress induced by doxorubicin may contribute to neurotoxicity, cognitive dysfunction, and accelerated brain aging in cancer patients and survivors. Peroxisomes might be a valuable new target for mitigating neuronal damage caused by chemotherapy drugs and for slowing down brain aging in general.
Indexed as
Identifiers
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.