ArticleAging2016
TFEB ameliorates the impairment of the autophagy-lysosome pathway in neurons induced by doxorubicin.
Article in Aging, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 55 citations in OpenAlex.
- Chemobrain as a Neuroimmune Syndrome: Mechanisms, Modifiers, and Emerging Multi-Target Therapeutic Strategies.Molecules (Basel, Switzerland) · 2026Review
- Mechanistic insights and therapeutic interventions of mitochondrial quality control in chemotherapy-related cognitive impairment.Neoplasia (New York, N.Y.) · 2026Review
- Enhancing the Water Solubility and Efficacy of Anticancer Drugs Using Hydroxypropyl-β-Cyclodextrin.International journal of molecular sciences · 2026Review
- The multifaceted mechanisms of Tanshinone IIA in doxorubicin-induced cardiotoxicity.Frontiers in medicine · 2026Review
- Different Mechanisms in Doxorubicin-Induced Neurotoxicity: Impact of BRCA Mutations.International journal of molecular sciences · 2025Review
- The challenge of chemotherapy-related cognitive impairment: assessing and managing cognitive decline after cancer treatment.Ecancermedicalscience · 2025Review
- Effect of Fangxia-Dihuang Decoction on doxorubicin-induced cognitive impairment in breast cancer animal model.Frontiers in oncology · 2025Article
- Wnt3a/GSK3β/β-catenin Signalling Modulates Doxorubicin-associated Memory Deficits in Breast Cancer.Molecular neurobiology · 2024Article
- Natural products for the treatment of chemotherapy-related cognitive impairment and prospects of nose-to-brain drug delivery.Frontiers in pharmacology · 2024Review
- A Pharmacological Review of Tanshinones, Naturally Occurring Monomers fromOxidative medicine and cellular longevity · 2023Review
- Stevia and Stevioside Attenuate Liver Steatosis through PPARα-Mediated Lipophagy inAntioxidants (Basel, Switzerland) · 2022Article
- Review
- Neurotoxic Effect of Doxorubicin Treatment on Cardiac Sympathetic Neurons.International journal of molecular sciences · 2022Article
- Chemobrain: mitoxantrone-induced oxidative stress, apoptotic and autophagic neuronal death in adult CD-1 mice.Archives of toxicology · 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
- Mechanisms of Chemotherapy-Induced Neurotoxicity.Frontiers in pharmacology · 2022Review
- Autophagy and the Lysosomal System in Cancer.Cells · 2021Review
- Article
- Oxidative Stress and Cognitive Alterations Induced by Cancer Chemotherapy Drugs: A Scoping Review.Antioxidants (Basel, Switzerland) · 2021Article
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 2 institutions in 1 country.
Funding
Abstract
Doxorubicin, a commonly used chemotherapy agent, induces severe cardio- and neurotoxicity. Molecular mechanisms of cardiotoxicity have been extensively studied, but mechanisms by which doxorubicin exhibits its neurotoxic properties remain unclear. Here, we show that doxorubicin impairs neuronal autophagy, leading to the accumulation of an autophagy substrate p62. Neurons treated with doxorubicin contained autophagosomes, damaged mitochondria, and lipid droplets. The brains from mice treated with pegylated liposomal doxorubicin exhibited autophagosomes, often with mitochondria, lipofuscin, and lipid droplets. Interestingly, lysosomes were less acidic in doxorubicin-treated neurons. Overexpression of the transcription factor EB (TFEB), which controls the autophagy-lysosome axis, increased survival of doxorubicin-treated neurons. 2-Hydroxypropyl-β-cyclodextrin (HPβCD), an activator of TFEB, also promoted neuronal survival, decreased the levels of p62, and lowered the pH in lysosomes. Taken together, substantial changes induced by doxorubicin contribute to neurotoxicity, cognitive disturbances in cancer patients and survivors, and accelerated brain aging. The TFEB pathway might be a new approach for mitigating damage of neuronal autophagy caused by doxorubicin.
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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.