ArticlePloS one2014
Trehalose reverses cell malfunction in fibroblasts from normal and Huntington's disease patients caused by proteosome inhibition.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 2 of them syntheses that pooled it.
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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
31 citing papers in PubMed, 2 syntheses or guidelines pooled it, 62 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition).Autophagy · 2016Guideline
- A double-blind, randomized, cross-over, placebo-controlled, pilot trial with Sativex in Huntington's disease.Journal of neurology · 2016Trial
- A clinical study and future prospects for bioactive compounds and semi-synthetic molecules in the therapies for Huntington's disease.Molecular neurobiology · 2024Review
- Neurodegenerative Diseases: New Hopes and Perspectives.Current molecular medicine · 2024Review
- Review
- The interplay between oxidative stress and autophagy: focus on the development of neurological diseases.Behavioral and brain functions : BBF · 2022Review
- Mitophagy and Neurodegeneration: Between the Knowns and the Unknowns.Frontiers in cell and developmental biology · 2022Review
- Autophagy and apoptosis cascade: which is more prominent in neuronal death?Cellular and molecular life sciences : CMLS · 2021Review
- Macroautophagy and Mitophagy in Neurodegenerative Disorders: Focus on Therapeutic Interventions.Biomedicines · 2021Review
- Natural compounds modulate the autophagy with potential implication of stroke.Acta pharmaceutica Sinica. B · 2021Review
- Enhancement of Autophagy and Solubilization of Ataxin-2 Alleviate Apoptosis in Spinocerebellar Ataxia Type 2 Patient Cells.Cerebellum (London, England) · 2020Article
- Analysis of In Vitro Cytotoxicity of Carbohydrate-Based Materials Used for Dissolvable Microneedle Arrays.Pharmaceutical research · 2020Article
- Therapeutic Advances for Huntington's Disease.Brain sciences · 2020Review
- Impaired Redox Signaling in Huntington's Disease: Therapeutic Implications.Frontiers in molecular neuroscience · 2019Review
- Autophagy induction by trehalose: Molecular mechanisms and therapeutic impacts.Journal of cellular physiology · 2018Review
- Proteostasis in Huntington's disease: disease mechanisms and therapeutic opportunities.Acta pharmacologica Sinica · 2018Review
- Trehalose reduces retinal degeneration, neuroinflammation and storage burden caused by a lysosomal hydrolase deficiency.Autophagy · 2018Article
- The cryoprotectant trehalose could inhibit ERS-induced apoptosis by activating autophagy in cryoprotected rat valves.PloS one · 2018Article
- Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntington's disease (HD) is a neurodegenerative disorder characterized by progressive motor, cognitive and psychiatric deficits, associated with predominant loss of striatal neurons and is caused by polyglutamine expansion in the huntingtin protein. Mutant huntingtin protein and its fragments are resistant to protein degradation and produce a blockade of the ubiquitin proteasome system (UPS). In HD models, the proteasome inhibitor epoxomicin aggravates protein accumulation and the inductor of autophagy, trehalose, diminishes it. We have investigated the effects of epoxomicin and trehalose in skin fibroblasts of control and HD patients. Untreated HD fibroblasts have increased the levels of ubiquitinized proteins and higher levels of reactive oxygen species (ROS), huntingtin and the autophagy marker LAMP2A. Baseline replication rates were higher in HD than in controls fibroblasts but that was reverted after 12 passages. Epoxomicin increases the activated caspase-3, HSP70, huntingtin, ubiquitinated proteins and ROS levels in both HD and controls. Treatment with trehalose counteracts the increase in ROS, ubiquitinated proteins, huntingtin and activated caspase-3 levels induced by epoxomicin, and also increases the LC3 levels more in HD fibroblast than controls. These results suggest that trehalose could revert protein processing abnormalities in patients with Huntington's Disease.
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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.