ArticleFrontiers in molecular neuroscience2017
Reversible Axonal Dystrophy by Calcium Modulation in Frataxin-Deficient Sensory Neurons of YG8R Mice.
Article in Frontiers in molecular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.
- Gene expression regulation by CaCellular & molecular biology letters · 2026Pooled it
- Autophagy activation by urolithin-a derivative UA-36 mitigates Friedreich's ataxia pathologies induced by frataxin deficiency.Molecular biomedicine · 2026Article
- Frataxin deficiency and the pathology of Friedreich's Ataxia across tissues.Tissue barriers · 2025Review
- Anatomical and functional analysis of the corticospinal tract in an FRDA mouse model.bioRxiv : the preprint server for biology · 2024Article
- Acute frataxin knockdown in induced pluripotent stem cell-derived cardiomyocytes activates a type I interferon response.Disease models & mechanisms · 2023Article
- Protein misfolding and clearance in the pathogenesis of a new infantile onset ataxia caused by mutations in PRDX3.Human molecular genetics · 2022Article
- Frataxin Deficit Leads to Reduced Dynamics of Growth Cones in Dorsal Root Ganglia Neurons of Friedreich's Ataxia YG8sR Model: A Multilinear Algebra Approach.Frontiers in molecular neuroscience · 2022Article
- Copper, Iron, and Manganese Toxicity in Neuropsychiatric Conditions.International journal of molecular sciences · 2021Review
- Selective Neuron Vulnerability in Common and Rare Diseases-Mitochondria in the Focus.Frontiers in molecular biosciences · 2021Review
- Oxidative stress modulates rearrangement of endoplasmic reticulum-mitochondria contacts and calcium dysregulation in a Friedreich's ataxia model.Redox biology · 2020Article
- Mitochondrial damage and senescence phenotype of cells derived from a novel frataxin G127V point mutation mouse model of Friedreich's ataxia.Disease models & mechanisms · 2020Article
- Antioxidant Therapies and Oxidative Stress in Friedreich´s Ataxia: The Right Path or Just a Diversion?Antioxidants (Basel, Switzerland) · 2020Review
- Hereditary Ataxia: A Focus on Heme Metabolism and Fe-S Cluster Biogenesis.International journal of molecular sciences · 2020Review
- Cofilin dysregulation alters actin turnover in frataxin-deficient neurons.Scientific reports · 2020Article
- Review
- Phosphodiesterase Inhibitors Revert Axonal Dystrophy in Friedreich's Ataxia Mouse Model.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019Article
- Transcriptional profiling of isogenic Friedreich ataxia neurons and effect of an HDAC inhibitor on disease signatures.The Journal of biological chemistry · 2019Article
- The Role of Iron in Friedreich's Ataxia: Insights From Studies in Human Tissues and Cellular and Animal Models.Frontiers in neuroscience · 2019Review
- Mitochondrial calcium signalling and neurodegenerative diseases.Neuronal signaling · 2018Review
- Impact ofInternational journal of molecular sciences · 2018Review
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Friedreich's ataxia (FRDA) is a peripheral neuropathy involving a loss of proprioceptive sensory neurons. Studies of biopsies from patients suggest that axonal dysfunction precedes the death of proprioceptive neurons in a dying-back process. We observed that the deficiency of frataxin in sensory neurons of dorsal root ganglia (DRG) of the YG8R mouse model causes the formation of axonal spheroids which retain dysfunctional mitochondria, shows alterations in the cytoskeleton and it produces impairment of axonal transport and autophagic flux. The homogenous distribution of axonal spheroids along the neurites supports the existence of continues focal damages. This lead us to propose for FRDA a model of distal axonopathy based on axonal focal damages. In addition, we observed the involvement of oxidative stress and dyshomeostasis of calcium in axonal spheroid formation generating axonal injury as a primary cause of pathophysiology. Axonal spheroids may be a consequence of calcium imbalance, thus we propose the quenching or removal extracellular Ca
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