Format

Send to

Choose Destination
EMBO Mol Med. 2019 Sep 5:e10473. doi: 10.15252/emmm.201910473. [Epub ahead of print]

Dyslipidemia in retinal metabolic disorders.

Author information

1
Department of Ophthalmology, Harvard Medical School, Boston Children's Hospital, Boston, MA, USA.
2
Manton Center for Orphan Disease, Harvard Medical School, Boston Children's Hospital, Boston, MA, USA.
3
National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA.
4
Department of Pediatrics, Pharmacology and Ophthalmology, CHU Sainte-Justine Research Center, Université de Montréal, Montreal, QC, Canada.
5
Department of Pharmacology and Therapeutics, University of Montreal, Montreal, QC, Canada.
6
Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
7
Center for Translational Vision Research, Gavin Herbert Eye Institute, Irvine, CA, USA.
8
Section for Ophthalmology, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Göteborg, Sweden.

Abstract

The light-sensitive photoreceptors in the retina are extremely metabolically demanding and have the highest density of mitochondria of any cell in the body. Both physiological and pathological retinal vascular growth and regression are controlled by photoreceptor energy demands. It is critical to understand the energy demands of photoreceptors and fuel sources supplying them to understand neurovascular diseases. Retinas are very rich in lipids, which are continuously recycled as lipid-rich photoreceptor outer segments are shed and reformed and dietary intake of lipids modulates retinal lipid composition. Lipids (as well as glucose) are fuel substrates for photoreceptor mitochondria. Dyslipidemia contributes to the development and progression of retinal dysfunction in many eye diseases. Here, we review photoreceptor energy demands with a focus on lipid metabolism in retinal neurovascular disorders.

KEYWORDS:

FGF21; dyslipidemia; photoreceptor; retinal metabolism; β-oxidation

PMID:
31486227
DOI:
10.15252/emmm.201910473
Free full text

Supplemental Content

Full text links

Icon for Wiley
Loading ...
Support Center