An interpretation of retinopathy of prematurity in terms of spindle cells: relationship to vitamin E prophylaxis and cryotherapy

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Abstract
Spindle cells in the hyperoxygenated, avascular, vanguard retina are proposed to be the peripheral inducers of the neovascularization associated with retinopathy of prematurity (ROP). The induction of ROP is conceptualized in terms of three basic events. First, activation of spindle cells results initially in the increase in gap junctions between adjacent spindle cells, secondarily in the increase in cytoplasmic volume of rough endoplasmic reticulum, and ultimately in the synthesis and secretion of angiogenic factors. Second, maturation of spindle cells is associated with a decrease in gap junctions, a diminished cytoplasmic volume of rough endoplasmic reticulum, and a cessation of synthesis and secretion of angiogenic factors. Third, myofibroblasts invade the vitreous concomitantly with spindle cell maturation and provide the tractional force that can produce retinal separation. The extent of interstitial retinol binding protein within the subretinal space explains the gestational-age-dependent efficacy of vitamin E in suppressing the development of severe ROP. The kinetics of both spindle cell activation/maturation and myofibroblast invasion predict the efficacy of appropriately timed and placed transretinal cryotherapy.