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.

中文翻译：

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3 型黄斑新生血管的临床病理特征和当前的动物模型。

3 型黄斑新血管形成 (MNV3) 或视网膜血管瘤增生 (RAP) 是一种独特类型的新血管年龄相关性黄斑变性 (AMD)，是老年人视力丧失的主要原因。在过去的十年中，对临床、多模态成像、组织病理学特征和治疗结果的系统研究为了解这种疾病提供了重要的新见解。这些研究支持 MNV3 起源于视网膜，并表明视网膜缺氧、炎症、von Hippel-Lindau (VHL)-缺氧诱导因子 (HIF)-血管内皮生长因子 (VEGF) 通路以及多种细胞类型参与了发育过程和 MNV3 的进展。几种小鼠模型，包括我组最近建立的Rb/p107/Vhl三重敲除小鼠模型，已经诱导了 MNV3 的许多组织学特征，并提供了对潜在病理机制的深入了解。这些模型揭示了视网膜缺氧、炎症、脂质代谢、VHL/HIF 通路和视网膜母细胞瘤肿瘤抑制因子 (Rb)-E2F 细胞周期通路在 MNV3 发展中的作用。本文将总结 MNV3 的临床、多模态成像和病理特征以及 MNV3 存在的动物模型的多样性，以及它们的优势和局限性。