TY - JOUR
T1 - Molecular mechanisms of subretinal fibrosis in age-related macular degeneration
AU - Ishikawa, Keijiro
AU - Kannan, Ram
AU - Hinton, David R.
N1 - Funding Information:
This work was supported by National Institutes of Health Grants EY03040 , EY01545 and the Arnold and Mabel Beckman Foundation and an unrestricted grant from Research to Prevent Blindness , New York, NY, 10022. K. Ishikawa is supported by a fellowship from the Japan Society for the Promotion of Science Postdoctoral Fellowships for Research Abroad. We thank Ernesto Barron and Christine Spee for technical assistance. The authors declare no conflicts of interest.
Publisher Copyright:
© 2015 Elsevier Ltd.
PY - 2014/10/26
Y1 - 2014/10/26
N2 - Subretinal fibrosis is a result of a wound healing response that follows choroidal neovascularization in neovascular age-related macular degeneration (nAMD). Although anti-vascular endothelial growth factor therapy has become a standard treatment that improves visual acuity in many nAMD patients, unsuccessful treatment outcomes have often been attributed to the progression of subretinal fibrosis. In this review, we summarize the cellular and extracellular components of subretinal fibrous membranes and also discuss the possible molecular mechanisms including the functional involvement of growth factors and the inflammatory response in the process. Moreover, we present an murine animal model of subretinal fibrosis that might facilitate greater understanding of the pathophysiology and the development of novel therapeutic strategies for the inhibition of subretinal fibrosis in nAMD.
AB - Subretinal fibrosis is a result of a wound healing response that follows choroidal neovascularization in neovascular age-related macular degeneration (nAMD). Although anti-vascular endothelial growth factor therapy has become a standard treatment that improves visual acuity in many nAMD patients, unsuccessful treatment outcomes have often been attributed to the progression of subretinal fibrosis. In this review, we summarize the cellular and extracellular components of subretinal fibrous membranes and also discuss the possible molecular mechanisms including the functional involvement of growth factors and the inflammatory response in the process. Moreover, we present an murine animal model of subretinal fibrosis that might facilitate greater understanding of the pathophysiology and the development of novel therapeutic strategies for the inhibition of subretinal fibrosis in nAMD.
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U2 - 10.1016/j.exer.2015.03.009
DO - 10.1016/j.exer.2015.03.009
M3 - Article
C2 - 25773985
AN - SCOPUS:84925261322
SN - 0014-4835
VL - 142
SP - 19
EP - 25
JO - Experimental Eye Research
JF - Experimental Eye Research
ER -