ArticleScientific reports2018
Frataxin overexpression in Müller cells protects retinal ganglion cells in a mouse model of ischemia/reperfusion injury in vivo.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- BDH1-Dependent Ketone Body Metabolism Maintains Müller Cell Homeostasis and Retinal Function.bioRxiv : the preprint server for biology · 2025Article
- Dysregulation of Mitochondrial Iron Regulators as a Basis of Iron-Mediated Retinal Degeneration in Rats.Neurotoxicity research · 2025Article
- Introducing a Porcine Inflammatory Ex Vivo Retina Model for Diabetic Retinopathy.International journal of molecular sciences · 2025Article
- Frataxin deficiency and the pathology of Friedreich's Ataxia across tissues.Tissue barriers · 2025Review
- Retinal Inflammation and Reactive Müller Cells: Neurotrophins' Release and Neuroprotective Strategies.Biology · 2024Review
- Effects of Iron and Zinc on Mitochondria: Potential Mechanisms of Glaucomatous Injury.Frontiers in cell and developmental biology · 2021Review
- A Novel HIF Inhibitor Halofuginone Prevents Neurodegeneration in a Murine Model of Retinal Ischemia-Reperfusion.International journal of molecular sciences · 2019Article
- Essential Roles of Lactate in Müller Cell Survival and Function.Molecular neurobiology · 2018Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Müller cells are critical for retinal function and neuronal survival but can become detrimental in response to retinal ischemia and increased oxidative stress. Elevated oxidative stress increases expression of the mitochondrial enzyme frataxin in the retina, and its overexpression is neuroprotective after ischemia. Whether frataxin expression in Müller cells might improve their function and protect neurons after ischemia is unknown. The aim of this study was to evaluate the effect of frataxin overexpression in Müller cells on neuronal survival after retinal ischemia/reperfusion in the mouse in vivo. Retinal ischemia/reperfusion was induced in mice overexpressing frataxin in Müller cells by transient elevation of intraocular pressure. Retinal ganglion cells survival was determined 14 days after lesion. Expression of frataxin, antioxidant enzymes, growth factors and inflammation markers was determined with qRT-PCR, Western blotting and immunohistochemistry 24 hours after lesion. Following lesion, there was a 65% increase in the number of surviving RGCs in frataxin overexpressing mice. Improved survival was associated with increased expression of the antioxidant enzymes Gpx1 and Sod1 as well as the growth factors Cntf and Lif. Additionally, microglial activation was decreased in these mice. Therefore, support of Müller cell function constitutes a feasible approach to reduce neuronal degeneration after ischemia.
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