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The adenosine A(2A) receptor (A(2A)R) modulates normal vascularization and pathologic angiogenesis in many tissues and may contribute to the pathogenesis of retinopathy of prematurity (ROP) characterized by abnormal retinal vascularization in surviving premature infants. Here, the authors studied the effects of the genetic inactivation of A(2A)R on normal retinal vascularization and the development of pathologic angiogenesis in oxygen-induced retinopathy (OIR), an animal model of ROP.

Genetic Inactivation of the Adenosine A2AReceptor Attenuates Pathologic but Not Developmental Angiogenesis in the Mouse Retina

Genetic Inactivation of the Adenosine A_2AReceptor Attenuates Pathologic but Not Developmental Angiogenesis in the Mouse Retina