Molecular mechanisms of subretinal fibrosis in age-related macular degeneration

Exp Eye Res. 2016 Jan:142:19-25. doi: 10.1016/j.exer.2015.03.009. Epub 2015 Mar 13.

Abstract

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.

Keywords: Epithelial–mesenchymal transition; Extracellular matrix; Growth factor; Laser-induced choroidal neovascularization; Macrophage; Matricellular protein; Myofibroblasts; Subretinal scar.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Angiogenesis Inhibitors / therapeutic use
  • Animals
  • Cytokines / metabolism
  • Disease Models, Animal
  • Epithelial-Mesenchymal Transition / physiology
  • Extracellular Matrix / metabolism
  • Fibrosis / complications*
  • Intercellular Signaling Peptides and Proteins / metabolism
  • Macular Degeneration* / drug therapy
  • Macular Degeneration* / immunology
  • Macular Degeneration* / metabolism
  • Macular Degeneration* / physiopathology
  • Mice
  • Molecular Targeted Therapy / methods
  • Retinal Pigment Epithelium / pathology

Substances

  • Angiogenesis Inhibitors
  • Cytokines
  • Intercellular Signaling Peptides and Proteins