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FGF21 Administration Suppresses Retinal and Choroidal Neovascularization in Mice

Journal article
Authors Z. J. Fu
Y. Gong
R. Liegl
Z. X. Wang
C. H. Liu
S. S. Meng
S. B. Burnim
N. J. Saba
T. W. Fredrick
P. C. Morss
Ann Hellström
S. Talukdar
L. E. H. Smith
Published in Cell Reports
Volume 18
Issue 7
Pages 1606-1613
ISSN 2211-1247
Publication year 2017
Published at Institute of Neuroscience and Physiology, Department of Clinical Neuroscience
Pages 1606-1613
Language en
Keywords proliferative diabetic-retinopathy, oxygen-induced retinopathy, endothelial growth-factor, brown adipose-tissue, macular degeneration, beta-klotho, tnf-alpha, adiponectin, type-2, prematurity, Cell Biology
Subject categories Ophthalmology, Cell biology


Pathological neovascularization, a leading cause of blindness, is seen in retinopathy of prematurity, diabetic retinopathy, and age-related macular degeneration. Using a mouse model of hypoxia-driven retinal neovascularization, wefind that fibroblast growth factor 21 (FGF21) administration suppresses, and FGF21 deficiency worsens, retinal neovessel growth. The protective effect of FGF21 against neovessel growth was abolished in adiponectin (APN)-deficient mice. FGF21 administration also decreased neovascular lesions in two models of neovascular age-related macular degeneration: very-low-density lipoprotein-receptor-deficient mice with retinal angiomatous proliferation and laser-induced choroidal neovascularization. FGF21 inhibited tumor necrosis alpha (TNF-alpha) expression but did not alter Vegfa expression in neovascular eyes. These data suggest that FGF21 may be a therapeutic target for pathologic vessel growth in patients with neovascular eye diseases, including retinopathy of prematurity, diabetic retinopathy, and age-related macular degeneration.

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