Mitochondrial Defects Drive Degenerative Retinal Diseases

被引：93

作者：

Ferrington, Deborah A. ^{[1
,2
]}

Fisher, Cody R. ^{[1
,2
]}

Kowluru, Renu A. ^{[3
]}

机构：

[1] Univ Minnesota, Dept Ophthalmol & Visual Neurosci, Minneapolis, MN 55455 USA

[2] Univ Minnesota, Grad Program Biochem Mol Biol & Biophys, Minneapolis, MN 55455 USA

[3] Wayne State Univ, Ophthalmol Vis & Anat Sci, Detroit, MI 48202 USA

来源：

TRENDS IN MOLECULAR MEDICINE | 2020年 / 26卷 / 01期

基金：

美国国家卫生研究院;

关键词：

PIGMENT EPITHELIAL-CELLS; MACULAR DEGENERATION; DIABETIC-RETINOPATHY; OXIDATIVE STRESS; TRANSCRIPTION FACTOR; PROGRESSIVE STAGES; DNA DAMAGE; PHOTOBIOMODULATION; PROTECTION; TRANSPORT;

D O I：

10.1016/j.molmed.2019.10.008

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Mitochondrial dysfunction is involved in the pathology of two major blinding retinal diseases, diabetic retinopathy (DR) and age-related macular degeneration (AMD). These diseases accumulate mitochondrial defects in distinct retinal subcellular structures, the vascular/neural network in DR and the retinal pigment epithelium (RPE) in AMD. These mitochondrial defects cause a metabolic crisis that drives disease. With no treatments to stop these diseases, coupled with an increasing population suffering from AMD and DR, there is an urgent need to develop new therapeutics targeting the mitochondria to prevent or reverse disease-specific pathology.

引用

页码：105 / 118

页数：14

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