ArticleScientific reports2017
Alterations in the carnitine cycle in a mouse model of Rett syndrome.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Evidence of neuronal DNA damage in the brains of patients with Rett syndrome.Disease models & mechanisms · 2025Article
- The epigenetic modification of DNA methylation in neurological diseases.Frontiers in immunology · 2024Review
- Cardiac Functional and Structural Abnormalities in a Mouse Model of CDKL5 Deficiency Disorder.International journal of molecular sciences · 2023Article
- QTPhysiological reports · 2022Article
- Delayed Ventricular Repolarization and Sodium Channel Current Modification in a Mouse Model of Rett Syndrome.International journal of molecular sciences · 2022Article
- Article
- Metabolic Signatures Differentiate Rett Syndrome From Unaffected Siblings.Frontiers in integrative neuroscience · 2020Article
- Potent hERG channel inhibition by sarizotan, an investigative treatment for Rett Syndrome.Journal of molecular and cellular cardiology · 2019Article
- Senescence Phenomena and Metabolic Alteration in Mesenchymal Stromal Cells from a Mouse Model of Rett Syndrome.International journal of molecular sciences · 2019Article
- New insights into Rett syndrome pathogenesis: defining the role of MEPC2 in DNA damage.Frontiers in neurologyReview
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rett syndrome (RTT) is a neurodevelopmental disease that leads to intellectual deficit, motor disability, epilepsy and increased risk of sudden death. Although in up to 95% of cases this disease is caused by de novo loss-of-function mutations in the X-linked methyl-CpG binding protein 2 gene, it is a multisystem disease associated also with mitochondrial metabolic imbalance. In addition, the presence of long QT intervals (LQT) on the patients' electrocardiograms has been associated with the development of ventricular tachyarrhythmias and sudden death. In the attempt to shed light on the mechanism underlying heart failure in RTT, we investigated the contribution of the carnitine cycle to the onset of mitochondrial dysfunction in the cardiac tissues of two subgroups of RTT mice, namely Mecp2
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