ArticleMetabolic brain disease2018
Mitochondrial alterations accompanied by oxidative stress conditions in skin fibroblasts of Huntington's disease patients.
Article in Metabolic brain disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 51 citations in OpenAlex.
- Induced pluripotent stem cells from a transgenic minipig model of Huntington's disease reveal early metabolic changes.Disease models & mechanisms · 2026Article
- Reversing Mitochondrial Dysfunction in Optineurin E50K Glaucoma: A Metabolic Approach to Neuroprotection.Research square · 2026Article
- Exploring the skin as an open window onto neurodegenerative diseases.Translational neurodegeneration · 2025Review
- Oxidative Stress in Huntington's Disease.Biomolecules · 2025Review
- Article
- Polyglutamine (PolyQ) Diseases: Navigating the Landscape of Neurodegeneration.ACS chemical neuroscience · 2024Review
- Mitochondrial targeted antioxidants as potential therapy for huntington's disease.Pharmacological reports : PR · 2024Review
- Correction of symptoms of Huntington disease by genistein through FOXO3-mediated autophagy stimulation.Autophagy · 2024Article
- Functional Characterisation of the Circular RNA,Cells · 2023Article
- Mitochondrial Bioenergy in Neurodegenerative Disease: Huntington and Parkinson.International journal of molecular sciences · 2023Review
- Biomolecular alterations detected in multiple sclerosis skin fibroblasts using Fourier transform infrared spectroscopy.Frontiers in cellular neuroscience · 2023Article
- Insights into Manganese Superoxide Dismutase and Human Diseases.International journal of molecular sciences · 2022Review
- Article
- Defective mitochondria-lysosomal axis enhances the release of extracellular vesicles containing mitochondrial DNA and proteins in Huntington's disease.Journal of extracellular biology · 2022Article
- Behavioral- and blood-based biomarkers for Huntington's disease: Studies on the R6/1 mouse model with prospects for early diagnosis and monitoring of the disease.Brain, behavior, & immunity - health · 2022Article
- The use of fibroblasts as a valuable strategy for studying mitochondrial impairment in neurological disorders.Translational neurodegeneration · 2022Review
- Review
- Neuroprotective effect of phospholipase AFrontiers in pharmacology · 2022Article
- Multiomic analysis on human cell model of wolfram syndrome reveals changes in mitochondrial morphology and function.Cell communication and signaling : CCS · 2021Article
- TFAM-deficient mouse skin fibroblasts - an ex vivo model of mitochondrial dysfunction.Disease models & mechanisms · 2021Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntington disease (HD) is an autosomal dominant neurodegenerative disorder manifesting as progressive impairment of motor function and different neuropsychiatric symptoms caused by an expansion of CAG repeats in huntingtin gene (HTT). Mitochondrial dysfunction and bioenergetic defects can contribute to the course of the disease, however, the molecular mechanism underlying this process is still largely unknown. In this study, we aimed to determine several mitochondrial parameters in HD fibroblasts and assess their relevance to the disease progression as well as to value mitochondrial pathology in peripheral cells as disease potential biomarker. We showed that HD fibroblasts demonstrate significantly lower growth rate compared to control fibroblasts despite the lack of cell cycle perturbations. In order to investigate mitochondrial contribution to cell growth differences between HD and healthy cells, we provided insight into various mitochondrial parameters. Conducted experiments have revealed a significant reduction of the ATP level in HD fibroblasts accompanied by a decrease in mitochondrial metabolic activity in relation to the cells from healthy donors. Importantly, there were no differences in the mitochondrial membrane potential (mtΔΨ) and OXPHOS complexes' levels. Slightly increased level of mitochondrial superoxide (mt. O
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