ArticleOxidative medicine and cellular longevity2014
Redox imbalance and morphological changes in skin fibroblasts in typical Rett syndrome.
Article in Oxidative medicine and cellular longevity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 64 citations in OpenAlex.
- Mapping of neuronal redox conditions in a mouse model of Rett syndrome.Neuroimage. Reports · 2025Article
- Evaluating the utility of growth differentiation factor 15 and fibroblast growth factor 21 as blood biomarkers for Rett syndrome.Scientific reports · 2025Article
- Optimized clonal isolation and immortalization of Rett syndrome patient fibroblasts for in vitro modeling of MECP2 mutations.Scientific reports · 2025Article
- p75NTR Modulation Reduces Oxidative Stress and the Expression of Pro-Inflammatory Mediators in a Cell Model of Rett Syndrome.Biomedicines · 2024Article
- Modelling phenotypes, variants and pathomechanisms of syndromic diseases in different systems.Medizinische Genetik : Mitteilungsblatt des Berufsverbandes Medizinische Genetik e.V · 2024Article
- Article
- Mitochondrial modulation with leriglitazone as a potential treatment for Rett syndrome.Journal of translational medicine · 2023Article
- Brain Mitochondrial Bioenergetics in Genetic Neurodevelopmental Disorders: Focus on Down, Rett and Fragile X Syndromes.International journal of molecular sciences · 2023Review
- An Example of Neuro-Glial Commitment and Differentiation of Muse Stem Cells Obtained from Patients withCells · 2023Article
- Oral Feeding of an Antioxidant Cocktail as a Therapeutic Strategy in a Mouse Model of Rett Syndrome: Merits and Limitations of Long-Term Treatment.Antioxidants (Basel, Switzerland) · 2022Article
- Article
- Energy metabolism in childhood neurodevelopmental disorders.EBioMedicine · 2021Review
- Altered Bone Status in Rett Syndrome.Life (Basel, Switzerland) · 2021Review
- MeCP2 deficiency exacerbates the neuroinflammatory setting and autoreactive response during an autoimmune challenge.Scientific reports · 2021Article
- The Relationship between Autism and Ehlers-Danlos Syndromes/Hypermobility Spectrum Disorders.Journal of personalized medicine · 2020Review
- 2,4 Dinitrophenol as Medicine.Cells · 2019Review
- Article
- Mitochondrial Electron Transport Chain Complex Dysfunction in MeCP2 Knock-Down Astrocytes: Protective Effects of Quercetin Hydrate.Journal of molecular neuroscience : MN · 2019Article
- Disclosing the functional changes of two genetic alterations in a patient with Chronic Progressive External Ophthalmoplegia: Report of the novel mtDNA m.7486G>A variant.Neuromuscular disorders : NMD · 2018Article
- Retention of Mitochondria in Mature Human Red Blood Cells as the Result of Autophagy Impairment in Rett Syndrome.Scientific reports · 2017Article
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Authors and funding
18 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Evidence of oxidative stress has been reported in the blood of patients with Rett syndrome (RTT), a neurodevelopmental disorder mainly caused by mutations in the gene encoding the Methyl-CpG-binding protein 2. Little is known regarding the redox status in RTT cellular systems and its relationship with the morphological phenotype. In RTT patients (n = 16) we investigated four different oxidative stress markers, F2-Isoprostanes (F2-IsoPs), F4-Neuroprostanes (F4-NeuroPs), nonprotein bound iron (NPBI), and (4-HNE PAs), and glutathione in one of the most accessible cells, that is, skin fibroblasts, and searched for possible changes in cellular/intracellular structure and qualitative modifications of synthesized collagen. Significantly increased F4-NeuroPs (12-folds), F2-IsoPs (7.5-folds) NPBI (2.3-folds), 4-HNE PAs (1.48-folds), and GSSG (1.44-folds) were detected, with significantly decreased GSH (-43.6%) and GSH/GSSG ratio (-3.05 folds). A marked dilation of the rough endoplasmic reticulum cisternae, associated with several cytoplasmic multilamellar bodies, was detectable in RTT fibroblasts. Colocalization of collagen I and collagen III, as well as the percentage of type I collagen as derived by semiquantitative immunofluorescence staining analyses, appears to be significantly reduced in RTT cells. Our findings indicate the presence of a redox imbalance and previously unrecognized morphological skin fibroblast abnormalities in RTT patients.
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