Protective or Harmful: The Dual Roles of Autophagy in Diabetic Retinopathy.

Protective or Harmful: The Dual Roles of Autophagy in Diabetic Retinopathy.
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保护还是有害:自噬在糖尿病视网膜病变中的双重作用。

DOI:
10.3389/fmed.2021.644121
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发表时间:
2021
影响因子:
3.9
通讯作者:
Xu X
Xu X
中科院分区:
医学3区
文献类型:
--
作者:
Gong Q;Wang H;Yu P;Qian T;Xu X

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自噬是一种涉及细胞内物质降解和回收的自降解途径。最近,这一过程因其对细胞、组织的生理过程和机体稳态维持的根本影响而引起了广泛的关注。自噬失调发生在一些疾病中,包括免疫疾病、癌症和神经退行性疾病。糖尿病视网膜病变(DR)作为糖尿病的一种严重微血管并发症,是导致全球工作年龄成年人视力丧失的主要原因。 DR的发病机制被认为与氧化应激积累、视网膜细胞凋亡、炎症反应、内质网(ER)应激和营养饥饿有关。这些因素与病理条件下自噬的调控密切相关。越来越多的证据表明自噬通过不同途径在 DR 进展中发挥潜在作用。然而,迄今为止,这种作用尚不清楚,并且自噬流水平的改变是否可以保护 DR,或者反而加剧进展,需要探索。在这篇综述中,我们探讨了 DR 条件下不同视网膜细胞和组织中自噬的变化和功能,并解释了 DR 进展的机制。我们的目标是为理解 DR 相关的应激调节自噬提供一个基础,并为未来 DR 的治疗干预提出新的靶点。
Autophagy is a self-degradative pathway involving intracellular substance degradation and recycling. Recently, this process has attracted a great deal of attention for its fundamental effect on physiological processes in cells, tissues, and the maintenance of organismal homeostasis. Dysregulation of autophagy occurs in some diseases, including immune disease, cancer, and neurodegenerative conditions. Diabetic retinopathy (DR), as a serious microvascular complication of diabetes, is the main cause of visual loss in working-age adults worldwide. The pathogenic mechanisms of DR are thought to be associated with accumulation of oxidative stress, retinal cell apoptosis, inflammatory response, endoplasmic reticulum (ER) stress, and nutrient starvation. These factors are closely related to the regulation of autophagy under pathological conditions. Increasing evidence has demonstrated the potential role of autophagy in the progression of DR through different pathways. However, to date this role is not understood, and whether the altered level of autophagy flux protects DR, or instead aggravates the progression, needs to be explored. In this review, we explore the alterations and functions of autophagy in different retinal cells and tissues under DR conditions, and explain the mechanisms involved in DR progression. We aim to provide a basis on which DR associated stress-modulated autophagy may be understood, and to suggest novel targets for future therapeutic intervention in DR.
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