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Clinical Pathological Features and Current Animal Models of Type 3 Macular Neovascularization
Type 3 macular neovascularization (MNV3), or retinal angiomatous proliferation (RAP), is a distinct type of neovascular age-related macular degeneration (AMD), which is a leading cause of vision loss in older persons. During the past decade, systematic investigation into the clinical, multimodal ima...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8427186/ https://www.ncbi.nlm.nih.gov/pubmed/34512255 http://dx.doi.org/10.3389/fnins.2021.734860 |
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author | Qiang, Wei Wei, Ran Chen, Yongjiang Chen, Danian |
author_facet | Qiang, Wei Wei, Ran Chen, Yongjiang Chen, Danian |
author_sort | Qiang, Wei |
collection | PubMed |
description | Type 3 macular neovascularization (MNV3), or retinal angiomatous proliferation (RAP), is a distinct type of neovascular age-related macular degeneration (AMD), which is a leading cause of vision loss in older persons. During the past decade, systematic investigation into the clinical, multimodal imaging, and histopathological features and therapeutic outcomes has provided important new insight into this disease. These studies favor the retinal origin of MNV3 and suggest the involvement of retinal hypoxia, inflammation, von Hippel–Lindau (VHL)–hypoxia-inducible factor (HIF)–vascular endothelial growth factor (VEGF) pathway, and multiple cell types in the development and progression of MNV3. Several mouse models, including the recently built Rb/p107/Vhl triple knockout mouse model by our group, have induced many of the histological features of MNV3 and provided much insight into the underlying pathological mechanisms. These models have revealed the roles of retinal hypoxia, inflammation, lipid metabolism, VHL/HIF pathway, and retinoblastoma tumor suppressor (Rb)–E2F cell cycle pathway in the development of MNV3. This article will summarize the clinical, multimodal imaging, and pathological features of MNV3 and the diversity of animal models that exist for MNV3, as well as their strengths and limitations. |
format | Online Article Text |
id | pubmed-8427186 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-84271862021-09-10 Clinical Pathological Features and Current Animal Models of Type 3 Macular Neovascularization Qiang, Wei Wei, Ran Chen, Yongjiang Chen, Danian Front Neurosci Neuroscience Type 3 macular neovascularization (MNV3), or retinal angiomatous proliferation (RAP), is a distinct type of neovascular age-related macular degeneration (AMD), which is a leading cause of vision loss in older persons. During the past decade, systematic investigation into the clinical, multimodal imaging, and histopathological features and therapeutic outcomes has provided important new insight into this disease. These studies favor the retinal origin of MNV3 and suggest the involvement of retinal hypoxia, inflammation, von Hippel–Lindau (VHL)–hypoxia-inducible factor (HIF)–vascular endothelial growth factor (VEGF) pathway, and multiple cell types in the development and progression of MNV3. Several mouse models, including the recently built Rb/p107/Vhl triple knockout mouse model by our group, have induced many of the histological features of MNV3 and provided much insight into the underlying pathological mechanisms. These models have revealed the roles of retinal hypoxia, inflammation, lipid metabolism, VHL/HIF pathway, and retinoblastoma tumor suppressor (Rb)–E2F cell cycle pathway in the development of MNV3. This article will summarize the clinical, multimodal imaging, and pathological features of MNV3 and the diversity of animal models that exist for MNV3, as well as their strengths and limitations. Frontiers Media S.A. 2021-08-26 /pmc/articles/PMC8427186/ /pubmed/34512255 http://dx.doi.org/10.3389/fnins.2021.734860 Text en Copyright © 2021 Qiang, Wei, Chen and Chen. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Neuroscience Qiang, Wei Wei, Ran Chen, Yongjiang Chen, Danian Clinical Pathological Features and Current Animal Models of Type 3 Macular Neovascularization |
title | Clinical Pathological Features and Current Animal Models of Type 3 Macular Neovascularization |
title_full | Clinical Pathological Features and Current Animal Models of Type 3 Macular Neovascularization |
title_fullStr | Clinical Pathological Features and Current Animal Models of Type 3 Macular Neovascularization |
title_full_unstemmed | Clinical Pathological Features and Current Animal Models of Type 3 Macular Neovascularization |
title_short | Clinical Pathological Features and Current Animal Models of Type 3 Macular Neovascularization |
title_sort | clinical pathological features and current animal models of type 3 macular neovascularization |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8427186/ https://www.ncbi.nlm.nih.gov/pubmed/34512255 http://dx.doi.org/10.3389/fnins.2021.734860 |
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