Increased Frataxin Levels Protect Retinal Ganglion Cells After Acute Ischemia/Reperfusion in the Mouse Retina In Vivo | Zendy

Rowena Schultz | Zendy; Otto W. Witte | Zendy; Christian Schmeer | Zendy

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Increased Frataxin Levels Protect Retinal Ganglion Cells After Acute Ischemia/Reperfusion in the Mouse Retina In Vivo

Author(s) -

Rowena Schultz,

Otto W. Witte,

Christian Schmeer

Publication year - 2016

Publication title -

investigative ophthalmology and visual science

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.935

H-Index - 218

eISSN - 1552-5783

pISSN - 0146-0404

DOI - 10.1167/iovs.16-19260

Subject(s) - neuroprotection , sod2 , frataxin , retinal ganglion cell , biology , ischemia , retinal , retina , oxidative stress , pathology , endocrinology , pharmacology , superoxide dismutase , microbiology and biotechnology , medicine , mitochondrion , biochemistry , neuroscience , aconitase

The mitochondrial protein frataxin (FXN) is highly expressed in metabolically active tissues and has been shown to improve cell survival in response to oxidative stress after ischemia. Retinal ischemia/hypoxia is a complication of ocular diseases such as diabetic retinopathy and glaucoma. There are no effective therapeutic approaches currently available. This study was performed to evaluate the neuroprotective effects of FXN after acute retinal ischemia/reperfusion in vivo.

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