Maintaining transparency: a review of the developmental physiology and pathophysiology of two avascular tissues.
The lens and cornea are transparent and usually avascular. Controlling nutrient supply while maintaining transparency is a physiological challenge for both tissues. During sleep and with contact lens wear the endothelial layer of the cornea may become hypoxic, compromising its ability to maintain corneal transparency. The mechanism responsible for establishing the avascular nature of the corneal stroma is unknown. In several pathological conditions, the stroma can be invaded by abnormal, leaky vessels, leading to opacification. Several molecules that are likely to help maintain the avascular nature of the corneal stroma have been identified, although their relative contributions remain to be demonstrated. The mammalian lens is surrounded by capillaries early in life. After the fetal vasculature regresses, the lens resides in a hypoxic environment. Hypoxia is likely to be required to maintain lens transparency. The vitreous body may help to maintain the low oxygen level around the lens. The hypothesis is presented that many aspects of the aging of the lens, including increased hardening, loss of accommodation (presbyopia), and opacification of the lens nucleus, are caused by exposure to oxygen. Testing this hypothesis may lead to prevention for nuclear cataract and insight into the mechanisms of lens aging. Although they are both transparent, corneal pathology is associated with an insufficient supply of oxygen, while lens pathology may involve excessive exposure to oxygen.
Beebe
David C
DC
Department of Ophthalmology and Visual Sciences, Washington University, St Louis, MO 63110, USA. beebe@wustl.edu
D000818:Animals; D002386:Cataract / Q000196:embryology / Q000209:etiology*; D016922:Cellular Senescence / Q000502:physiology; D003315:Cornea / Q000098:blood supply* / Q000196:embryology* / Q000502:physiology; D047109:Fetal Development / Q000502:physiology; D005502:Food; D006801:Humans; D007908:Lens, Crystalline / Q000098:blood supply* / Q000196:embryology* / Q000502:physiology; D008833:Microcirculation / Q000502:physiology; D008954:Models, Biological; D018919:Neovascularization, Physiologic / Q000502:physiology; D010100:Oxygen / Q000009:adverse effects; D010101:Oxygen Consumption / Q000502:physiology
D010100:Oxygen