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Chapter 73 – Retinal energy metabolism

Robert A Linsenmeier

Clinical background (Box 73.1)

Altered retinal oxygenation plays a central role in the pathogenesis of many retinal diseases and a hypothesized role in others.[1] Unfortunately, despite decades of work in some cases, the precise role of oxygen in certain complex diseases remains elusive.

Box 73.1 

Selected roles of hypoxia in retinal disease

Retinal diseases are complex, but hypoxia contributes to many:
      Diabetic retinopathy: hypoxia due to capillary loss in preproliferative retinopathy contributes to neovascularization. Possible hypoxia in background retinopathy
      Retinopathy of prematurity: hypoxia following end of oxygen supplementation contributes to neovascularization
      Central or branch retinal artery occlusion: choroidal supply cannot compensate for the lack of retinal circulation, leading to cell death in the inner retina
      Retinal detachment: separation of retina from choroidal circulation reduces flux of oxygen to photoreceptors
      Age-related macular degeneration: reduced choroidal blood flow and impaired transport may contribute to upregulation of vascular endothelial growth factor
      Glaucoma: reduced blood flow to the optic nerve head may contribute to hypoxia and the loss of retinal ganglion cells

There are three different categories of situations in which oxygen can play a critical role in disease. First, and most obvious, are situations involving ischemia. Because oxygen is usually the limiting substrate for metabolism, and cannot be stored, even a short-term loss of oxygen leads to devastating consequences in conditions such as central or branch retinal artery occlusion ( Chapter 63). Ischemia is certainly involved in other cases, such as after capillary dropout in diabetes (Chapters 65 and 66Chapter 65 Chapter 66). These conditions involve anoxia, because there is essentially no redundancy or safety factor in the retinal circulation where one …