Department of Ophthalmology, Visual and Anatomical Sciences, Wayne State University, Detroit, MI 48201, USA.
Cells. 2023 Jan 12;12(2):300. doi: 10.3390/cells12020300.
Diabetic retinopathy, one of the most devastating complications of diabetes, is a multifactorial progressing disease with a very complex etiology. Although many metabolic, molecular, functional and structural changes have been identified in the retina and its vasculature, the exact molecular mechanism of its pathogenesis still remains elusive. Sustained high-circulating glucose increases oxidative stress in the retina and also activates the inflammatory cascade. Free radicals increase inflammatory mediators, and inflammation can increase production of free radicals, suggesting a positive loop between them. In addition, diabetes also facilitates many epigenetic modifications that can influence transcription of a gene without changing the DNA sequence. Several genes associated with oxidative stress and inflammation in the pathogenesis of diabetic retinopathy are also influenced by epigenetic modifications. This review discusses cross-talks between oxidative stress, inflammation and epigenetics in diabetic retinopathy. Since epigenetic changes are influenced by external factors such as environment and lifestyle, and they can also be reversed, this opens up possibilities for new strategies to inhibit the development/progression of this sight-threatening disease.
糖尿病性视网膜病变是糖尿病最具破坏性的并发症之一，是一种多因素进行性疾病，其病因非常复杂。尽管在视网膜及其血管中已经发现了许多代谢、分子、功能和结构上的改变，但它的确切发病机制的分子机制仍然难以捉摸。持续的高循环葡萄糖会增加视网膜中的氧化应激，也会激活炎症级联反应。自由基增加炎症介质，炎症可以增加自由基的产生，这表明它们之间存在正反馈环。此外，糖尿病还促进了许多表观遗传修饰，这些修饰可以在不改变 DNA 序列的情况下影响基因的转录。一些与糖尿病性视网膜病变发病机制中的氧化应激和炎症相关的基因也受到表观遗传修饰的影响。本文综述了糖尿病性视网膜病变中氧化应激、炎症和表观遗传学之间的相互作用。由于表观遗传变化受环境和生活方式等外部因素的影响，并且可以逆转，这为抑制这种威胁视力的疾病的发展/进展提供了新的策略的可能性。
