ArticlePloS one2015
TORC1 Inhibition by Rapamycin Promotes Antioxidant Defences in a Drosophila Model of Friedreich's Ataxia.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 51 citations in OpenAlex.
- Hypomagnetic Field Exposure Alters Iron-Sulfur Homeostasis and Oxidative Balance in a Frataxin-Deficient Insect System.Insects · 2026Article
- Rapamycin and Post-Deficiency Dietary Recovery Reshape Antioxidant Response and Survival in Offspring of Iron-Deficient Mothers.Biological trace element research · 2025Article
- Review
- Valproic acid and/or rapamycin preconditioning protects hair follicle stem cells from oxygen glucose serum deprivation-induced oxidative injury via activating Nrf2 pathway.Molecular biology research communications · 2024Article
- Article
- Hyperactivation of mTOR and AKT in a cardiac hypertrophy animal model of Friedreich ataxia.Heliyon · 2022Article
- Brain-protective mechanisms of autophagy associated circRNAs: Kick starting self-cleaning mode in brain cellsFrontiers in molecular neuroscience · 2022Review
- A Multidrug Approach to Modulate the Mitochondrial Metabolism Impairment and Relative Oxidative Stress in Fanconi Anemia Complementation Group A.Metabolites · 2021Article
- Impaired antioxidant KEAP1-NRF2 system in amyotrophic lateral sclerosis: NRF2 activation as a potential therapeutic strategy.Molecular neurodegeneration · 2021Review
- G6PD deficiency, redox homeostasis, and viral infections: implications for SARS-CoV-2 (COVID-19).Free radical research · 2021Review
- Effect of Calcineurin Inhibitors and Mammalian Target of Rapamycin Inhibitors on the Course of COVID-19 in Kidney Transplant Recipients.Annals of transplantation · 2021Review
- Thioredoxin and Glutaredoxin Systems as Potential Targets for the Development of New Treatments in Friedreich's Ataxia.Antioxidants (Basel, Switzerland) · 2020Review
- Antioxidant Therapies and Oxidative Stress in Friedreich´s Ataxia: The Right Path or Just a Diversion?Antioxidants (Basel, Switzerland) · 2020Review
- Rapamycin attenuates the paraquat-induced pulmonary fibrosis through activating Nrf2 pathway.Journal of cellular physiology · 2020Article
- Noninvasive Cerebellar Stimulation as a Complement Tool to Pharmacotherapy.Current neuropharmacology · 2019Review
- The role of Nrf2 signaling in counteracting neurodegenerative diseases.The FEBS journal · 2018Review
- Impact ofInternational journal of molecular sciences · 2018Review
- The role of oxidative stress in Friedreich's ataxia.FEBS letters · 2018Review
- Everolimus, a mammalian target of rapamycin inhibitor, ameliorated streptozotocin-induced learning and memory deficits via neurochemical alterations in male rats.EXCLI journal · 2018Article
- Experimental Models for Aging and their Potential for Novel Drug Discovery.Current neuropharmacology · 2018Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Friedreich's ataxia (FRDA), the most common inherited ataxia in the Caucasian population, is a multisystemic disease caused by a significant decrease in the frataxin level. To identify genes capable of modifying the severity of the symptoms of frataxin depletion, we performed a candidate genetic screen in a Drosophila RNAi-based model of FRDA. We found that genetic reduction in TOR Complex 1 (TORC1) signalling improves the impaired motor performance phenotype of FRDA model flies. Pharmacologic inhibition of TORC1 signalling by rapamycin also restored this phenotype and increased the lifespan and ATP levels. Furthermore, rapamycin reduced the altered levels of malondialdehyde + 4-hydroxyalkenals and total glutathione of the model flies. The rapamycin-mediated protection against oxidative stress is due in part to an increase in the transcription of antioxidant genes mediated by cap-n-collar (Drosophila ortholog of Nrf2). Our results suggest that autophagy is indeed necessary for the protective effect of rapamycin in hyperoxia. Rapamycin increased the survival and aconitase activity of model flies subjected to high oxidative insult, and this improvement was abolished by the autophagy inhibitor 3-methyladenine. These results point to the TORC1 pathway as a new potential therapeutic target for FRDA and as a guide to finding new promising molecules for disease treatment.
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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.