The role of microglia in the development of diabetic retinopathy and its potential clinical application.

IF 3.4 3区 生物学 Q3 CELL BIOLOGY
Tingting Lu, Jiameng Shang, Shengdan Pu, Yuxin Xu, Xiaotong Sun, Xinyuan Gao
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Abstract

Lately, research on the function of microglia in diabetic retinopathy (DR) is becoming increasingly focused. Microglia are immune cells that dwell in the central nervous system and are crucial to the pathophysiology of DR. According to studies, a hyperglycemic environment can activate microglia, bringing them out of a resting state to an active state. This allows them to release a variety of inflammatory factors and chemokines, which can then cause retinal inflammatory reactions. When it comes to angiogenesis in DR, activated microglia release a variety of angiogenic substances, such as vascular endothelial growth factor (VEGF), to create aberrant new blood vessels. Moreover, microglia contribute to the retina's oxidative stress process by generating and releasing reactive oxygen and nitrogen-free radicals, which exacerbates retinal damage. Researchers have proposed a variety of strategies for the activation of microglia and the inflammatory response it triggers. By inhibiting the excessive activation of microglia and reducing the release of inflammatory factors, the inflammatory response and damage to the retina can be alleviated. Drugs that interfere with retinal microglia can also be used to regulate vascular damage and inhibit the formation of new blood vessels. In addition, antioxidants are used to remove reactive oxygen and free radicals, reduce oxidative stress levels, and protect retinal cells. These therapeutic strategies aim to achieve the purpose of treating DR by regulating the function of microglia. Thus, we highlight the possibility that therapy aimed at microglia could offer fresh ideas for treating DR.

小胶质细胞在糖尿病视网膜病变发展中的作用及其潜在的临床应用。
近年来,关于小胶质细胞在糖尿病视网膜病变(DR)中的作用的研究越来越受到关注。小胶质细胞是中枢神经系统中的免疫细胞,对dr的病理生理至关重要。根据研究,高血糖环境可以激活小胶质细胞,使其从静止状态进入活跃状态。这使它们能够释放各种炎症因子和趋化因子,然后引起视网膜炎症反应。当涉及到DR的血管生成时,激活的小胶质细胞释放多种血管生成物质,如血管内皮生长因子(VEGF),以产生异常的新血管。此外,小胶质细胞通过产生和释放活性氧和无氮自由基来促进视网膜的氧化应激过程,从而加剧视网膜损伤。研究人员提出了多种策略来激活小胶质细胞及其引发的炎症反应。通过抑制小胶质细胞的过度激活,减少炎症因子的释放,可以减轻炎症反应和对视网膜的损伤。干扰视网膜小胶质细胞的药物也可以用来调节血管损伤和抑制新血管的形成。此外,抗氧化剂用于去除活性氧和自由基,降低氧化应激水平,保护视网膜细胞。这些治疗策略旨在通过调节小胶质细胞的功能来达到治疗DR的目的。因此,我们强调针对小胶质细胞的治疗可能为治疗DR提供新的思路。
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来源期刊
Human Cell
Human Cell CELL BIOLOGY-
CiteScore
5.90
自引率
2.30%
发文量
176
审稿时长
4.5 months
期刊介绍: Human Cell is the official English-language journal of the Japan Human Cell Society. The journal serves as a forum for international research on all aspects of the human cell, encompassing not only cell biology but also pathology, cytology, and oncology, including clinical oncology. Embryonic stem cells derived from animals, regenerative medicine using animal cells, and experimental animal models with implications for human diseases are covered as well. Submissions in any of the following categories will be considered: Research Articles, Cell Lines, Rapid Communications, Reviews, and Letters to the Editor. A brief clinical case report focusing on cellular responses to pathological insults in human studies may also be submitted as a Letter to the Editor in a concise and short format. Not only basic scientists but also gynecologists, oncologists, and other clinical scientists are welcome to submit work expressing new ideas or research using human cells.
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