Publication: Power to see—Drivers of aerobic glycolysis in the mammalian retina: A review
Issued Date
2020-01-01
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ISSN
14429071
14426404
14426404
Other identifier(s)
2-s2.0-85089453875
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Mahidol University
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SCOPUS
Bibliographic Citation
Clinical and Experimental Ophthalmology. (2020)
Suggested Citation
Cameron D. Haydinger, Thaksaon Kittipassorn, Daniel J. Peet Power to see—Drivers of aerobic glycolysis in the mammalian retina: A review. Clinical and Experimental Ophthalmology. (2020). doi:10.1111/ceo.13833 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/58215
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Title
Power to see—Drivers of aerobic glycolysis in the mammalian retina: A review
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Abstract
© 2020 Royal Australian and New Zealand College of Ophthalmologists The mammalian retina converts most glucose to lactate rather than catabolizing it completely to carbon dioxide via oxidative phosphorylation, despite the availability of oxygen. This unusual metabolism is known as aerobic glycolysis or the Warburg effect. Molecules and pathways that drive aerobic glycolysis have been identified and thoroughly studied in the context of cancer but remain relatively poorly understood in the retina. Here, we review recent research on the molecular mechanisms that underly aerobic glycolysis in the retina, focusing on key glycolytic enzymes including hexokinase 2 (HK2), pyruvate kinase M2 (PKM2) and lactate dehydrogenase A (LDHA). We also discuss the potential involvement of cell signalling and transcriptional pathways including phosphoinositide 3-kinase (PI3K) signalling, fibroblast growth factor receptor (FGFR) signalling, and hypoxia-inducible factor 1 (HIF-1), which have been implicated in driving aerobic glycolysis in the context of cancer.