Journal
ISCIENCE
Volume 23, Issue 11, Pages -Publisher
CELL PRESS
DOI: 10.1016/j.isci.2020.101672
Keywords
-
Categories
Funding
- NIH [EY026030, EY029806, EY022645]
- Retina Research Foundation
- BrightFocus Foundation
- Orphan Disease Center, University of Pennsylvania [MDBR-19-130-CRB1]
- WV INBRE grant [P20 GM103434]
- WVCTSI [GM104942]
- Australian NHMRC [APP1145121]
- Lowy Medical Research Institute
- Australian NHMRC practitioner fellowship
Ask authors/readers for more resources
Photoreceptors, especially cones, which are enriched in the human macula, have high energy demands, making them vulnerable to metabolic stress. Metabolic dysfunction of photoreceptors and their supporting retinal pigment epithelium (RPE) is an important underlying cause of degenerative retinal diseases. However, how cones and the macula support their exorbitant metabolic demand and communicate with RPE is unclear. By profiling metabolite uptake and release and analyzing metabolic genes, we have found cone-rich retinas and human macula share specific metabolic features with upregulated pathways in pyruvate metabolism, mitochondrial TCA cycle, and lipid synthesis. Human neural retina and RPE have distinct but complementary metabolic features. Retinal metabolism centers on NADH production and neurotransmitter biosynthesis. The retina needs aspartate to sustain its aerobic glycolysis and mitochondrial metabolism. RPE metabolism is directed toward NADPH production and biosynthesis of acetyl-rich metabolites, serine, and others. RPE consumes multiple nutrients, including proline, to produce metabolites for the retina.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available