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Stimulation of AMPK prevents degeneration of photoreceptors and the retinal pigment epithelium
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Stimulation of AMPK prevents degeneration of photoreceptors and the retinal pigment epithelium
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Journal Article
Stimulation of AMPK prevents degeneration of photoreceptors and the retinal pigment epithelium
2018
Overview
Retinal degenerative diseases are generally characterized by a permanent loss of light-sensitive retinal neurons known as photoreceptors, or their support cells, the retinal pigmented epithelium (RPE). Metabolic dysfunction has been implicated as a common mechanism of degeneration. In this study, we used the drug metformin in a gain-of-function approach to activate adenosine monophosphate-activated protein kinase (AMPK). We found that treatment protected photoreceptors and the RPE from acute injury and delayed inherited retinal degeneration. Protection was associated with decreased oxidative stress, decreased DNA damage, and increased mitochondrial energy production. To determine whether protection was a local or a systemic effect of metformin, we used AMPK retinal knockout mice and found that local expression of AMPK catalytic subunit α2 was required for metformin-induced protection. Our data demonstrate that increasing the activity of AMPK in retinal neurons or glia can delay or prevent degeneration of photoreceptors and the RPE from multiple types of cell-death triggers.
Publisher
National Academy of Sciences
Subject
/ AMP
/ AMP-Activated Protein Kinases - physiology
/ Animals
/ DNA
/ Female
/ Hypoglycemic Agents - pharmacology
/ Male
/ Mice
/ Neurons
/ Oxidative Stress - drug effects
/ Photoreceptor Cells - drug effects
/ Photoreceptor Cells - metabolism
/ Proteins
/ Retina
/ Retinal Degeneration - metabolism
/ Retinal Degeneration - pathology
/ Retinal Degeneration - prevention & control
