ArticleRedox biology2020
Oxidative stress modulates rearrangement of endoplasmic reticulum-mitochondria contacts and calcium dysregulation in a Friedreich's ataxia model.
Article in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
35 citing papers in PubMed, 49 citations in OpenAlex.
- CTCF-FXN regulatory axis plays critical roles in clinical assessments and disease progression of primary open-angle glaucoma.Journal of molecular medicine (Berlin, Germany) · 2026Article
- BRD4-mediated ER membrane contact creates functionally distinct mitochondrial subtypes.Molecular cell · 2026Article
- Mitochondria-endoplasmic reticulum contact sites in hepatocytic senescence.Cellular & molecular biology letters · 2026Review
- Structural and Functional Alterations of MAMs and Their Immunomodulatory Roles in Sepsis-Induced Lung Injury.Journal of immunology research · 2026Review
- Cerebellar deep brain stimulation rescues Purkinje cell mitochondrial density in a genetic mouse model of cerebellar ataxia.Brain research bulletin · 2026Article
- Review
- Autosomal Recessive Cerebellar Ataxias: Translating Genes to Therapies.Annals of neurology · 2025Review
- Mitochondrial Complex I and ROS control neuromuscular function through opposing pre- and postsynaptic mechanisms.PLoS biology · 2025Article
- Mitochondrial Complex I and ROS control neuromuscular function through opposing pre- and postsynaptic mechanisms.bioRxiv : the preprint server for biology · 2025Article
- Mitochondria-Associated Membranes: A Key Point of Neurodegenerative Diseases.CNS neuroscience & therapeutics · 2025Review
- Mitochondria-associated endoplasmic reticulum membranes and myocardial ischemia: from molecular mechanisms to therapeutic strategies.Journal of translational medicine · 2025Review
- Cardiomyocyte-specific Piezo1 deficiency mitigates ischemia-reperfusion injury by preserving mitochondrial homeostasis.Redox biology · 2025Article
- Mechanisms of cellular senescence-induced vascular aging: evidence of senotherapeutic strategies.The journal of cardiovascular aging · 2025Article
- Decoding Nucleotide Repeat Expansion Diseases: Novel Insights fromInternational journal of molecular sciences · 2024Review
- TBC1D15-regulated mitochondria-lysosome membrane contact exerts neuroprotective effects by alleviating mitochondrial calcium overload in seizure.Scientific reports · 2024Article
- Mitochondrial Calcium Regulation of Cardiac Metabolism in Health and Disease.Physiology (Bethesda, Md.) · 2024Review
- A promising anti-tumor targeting on ERMMDs mediated abnormal lipid metabolism in tumor cells.Cell death & disease · 2024Review
- Gene editing improves endoplasmic reticulum-mitochondrial contacts and unfolded protein response in Friedreich's ataxia iPSC-derived neurons.Frontiers in pharmacology · 2024Article
- Mitochondrial Inherited Disorders and their Correlation with Neurodegenerative Diseases.Endocrine, metabolic & immune disorders drug targets · 2024Review
- Emerging antioxidant therapies in Friedreich's ataxia.Frontiers in pharmacology · 2024Review
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
Abstract
Friedreich ataxia (FRDA) is a neurodegenerative disorder characterized by neuromuscular and neurological manifestations. It is caused by mutations in the FXN gene, which results in loss of the mitochondrial protein frataxin. Endoplasmic Reticulum-mitochondria associated membranes (MAMs) are inter-organelle structures involved in the regulation of essential cellular processes, including lipid metabolism and calcium signaling. In the present study, we have analyzed in both, unicellular and multicellular models of FRDA, calcium management and integrity of MAMs. We observed that function of MAMs is compromised in our cellular model of FRDA, which was improved upon treatment with antioxidants. In agreement, promoting mitochondrial calcium uptake was sufficient to restore several defects caused by frataxin deficiency in Drosophila Melanogaster. Remarkably, our findings describe for the first time frataxin as a member of the protein network of MAMs, where interacts with two of the main proteins implicated in endoplasmic reticulum-mitochondria communication. These results suggest a new role of frataxin, indicate that FRDA goes beyond mitochondrial defects and highlight MAMs as novel therapeutic candidates to improve patient's conditions.
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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.