Müller细胞胶质间质转化在视网膜纤维化疾病中的作用
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国家区域医疗中心 江苏省人民医院宿迁医院(宿迁市第一人民医院) 南京医科大学附属宿迁第一人民医院

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宿迁市自然科学基金项目(No.K202312) 南京医科大学科技发展基金项目(No.NMUB20220215)


Roles of Müller glial-mesenchymal transition in pathogenesis of retinal fibrosis diseases
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1.National Regional Medical Center;2.Suqian Hospital, Jiangsu province hospital (Suqian First People’s Hospital);3.the Affiliated Suqian First People’s Hospital of Nanjing Medical University

Fund Project:

Natural Science Foundation of Suqian (No.K202312) Science and technology Development Foundation of Nanjing Medical University (No.NMUB20220215)

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    摘要:

    胶质间质转化(GMT)指胶质细胞在各种因素刺激下逐渐获得间质细胞表型和特征的生物学过程,与视网膜纤维化疾病密切相关。Müller细胞是视网膜上最主要的大胶质细胞,在受到各种病理因素刺激时被激活并发生转分化。目前,已有研究表明,Müller细胞GMT与糖尿病视网膜病变、特发性黄斑前膜(iERM)、增生性玻璃体视网膜病变(PVR)、年龄相关性黄斑变性(AMD)等多种疾病密切相关。尽管GMT相关调控机制尚不完全明确,但作为一个潜在的干预靶点,具有良好的研究前景。了解Müller细胞GMT在视网膜疾病中的研究进展,对于全面揭示细胞转型机制在视网膜疾病中的交互作用网络具有重要意义,有望探索出一条新的治疗策略,为相关患者的治疗带来突破。

    Abstract:

    Glial-mesenchymal transition (GMT) refers to the biological process in which glial cells gradually adopt the phenotypic of characteristics mesenchymal cells under the stimulation of various factors, which is closely associated with retinal fibrosis diseases. Müller cells are the major retinal macroglia, activated in response to a variety of stimuli and in different pathological conditions, and transdifferentiation ensues. Studies have shown that GMT is closely related to various diseases such as diabetic retinopathy (DR), idiopathic epiretinal membrane (iERM), age-related macular degeneration (AMD), proliferative vitreoretinopathy (PVR). Although the regulatory mechanism involved GMT remains elusive, it has an emerging research prospect as a potential intervention target. Understanding the research progress of Müller GMT in retinal diseases is of great significance to fully reveal the interaction network of cell transdifferentiation mechanism in retinal diseases, and it is expected to explore a new treatment strategy and bring breakthroughs for the treatment of related patients.

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  • 收稿日期:2024-01-03
  • 最后修改日期:2024-03-13
  • 录用日期:2024-04-22
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