Preventing pathological regression of blood vessels

Abstract

Oxygen administration to premature infants suppresses retinal VEGF expression and results in the catastrophic vessel loss associated with retinopathy of prematurity. A study investigating the development of the retinal vasculature in mice (see related article on pages 50–57) demonstrates that specific activation of VEGF receptor-1 by placental growth factor-1 protects against oxygen-induced vessel loss without stimulating vascular proliferation and neovascularization.

Figure 1

ROP pathogenesis and suggested treatments. (a) Retina vessels in the process of their formation and progressive covering of the retina surface. (b) Hyperoxia at this formative stage suppresses VEGF and, consequently, results in regression of newly formed vessels. (c) Upon return to normal air, the ischemic retina upregulates VEGF to high levels, causing excessive formation of leaky vessels. To antagonize VEGF at this stage has been suggested as a strategy to reduce adverse vessel formation. (d) An alternative strategy proposed by Shih et al. (2) is to protect retina vessels from oxygen-induced obliteration through administration of PlGF-1.