Abstract
Age-related macular degeneration (AMD) is the leading cause of blindness in the elderly in developed countries. Neovascular AMD (nAMD) accounts for 90% of AMD-related vision loss. Although intravitreal injection of VEGF inhibitors can improve vision in nAMD, approximately 1/3 of patients do not benefit from the therapy due to macular fibrosis. The molecular mechanism underlying the transition of the neovascular lesion to a fibrovascular phenotype remains unknown. Here we discussed the clinical features and risk factors of macular fibrosis secondary to nAMD. Myofibroblasts are key cells in fibrosis development. However, fibroblasts do not exist in the macula. Potential sources of myofibroblast precursors, the molecular cues in the macular microenvironment that recruit them and the pathways that control their differentiation and activation in macular fibrosis were also discussed. Furthermore, we highlighted the challenges in macular fibrosis research and the urgent need for better animal models for mechanistic and therapeutic studies.
Original language | English |
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Pages (from-to) | 283-291 |
Number of pages | 9 |
Journal | EBioMedicine |
Volume | 38 |
Early online date | 22 Nov 2018 |
DOIs | |
Publication status | Published - 01 Dec 2018 |
Keywords
- Age-related macular degeneration
- Inflammation
- Macular fibrosis
- Myofibroblast
- Risk factors
ASJC Scopus subject areas
- General Biochemistry,Genetics and Molecular Biology
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Investigating the role of the complement system in the pathogenesis of sub-retinal fibrosis in neovascular age related macular degeneration
Little, K. (Author), Chen, M. (Supervisor) & Xu, H. (Supervisor), Jul 2020Student thesis: Doctoral Thesis › Doctor of Philosophy