Panjab University, Department of Biochemistry, Basic Medical Science Block II, Chandigarh 160014, India.
Oxid Med Cell Longev. 2019 Mar 6;2019:8458472. doi: 10.1155/2019/8458472. eCollection 2019.
Diabetic retinopathy (DR) is a vascular insult that accompanies the hyperglycemic state. Retinal vasculature holds a pivotal role in maintaining the integrity of the retina, and any alteration to retinal vasculature affects retinal functions. The blood retinal barrier, a prerequisite to vision acuity, is most susceptible to damage during the progression of DR. This is a consequence of impaired biochemical pathways such as the polyol, advanced end glycation products (AGE), hexosamine, protein kinase C (PKC), and tissue renin-angiotensin system (RAS) pathways. Moreover, the role of histone modification and altered miRNA expression is also emerging as a major contributor. Epigenetic changes create a link between altered protein function and redox status of retinal cells, creating a state of metabolic memory. Although various biochemical pathways underlie the etiology of DR, the major insult to the retina is due to oxidative stress, a unifying factor of altered biochemical pathways. This review primarily focuses on the critical biochemical pathways altered in DR leading to vascular dysfunctions and discusses antioxidants as plausible treatment strategies.
糖尿病视网膜病变（DR）是一种伴随高血糖状态的血管损伤。视网膜血管在维持视网膜完整性方面起着关键作用，任何对视网膜血管的改变都会影响视网膜功能。作为视力敏锐度的先决条件，血视网膜屏障在 DR 的进展过程中最容易受到损害。这是由于多元醇、晚期糖基化终产物（AGE）、己糖胺、蛋白激酶 C（PKC）和组织肾素-血管紧张素系统（RAS）途径等生化途径受损所致。此外，组蛋白修饰和 miRNA 表达改变的作用也越来越明显。表观遗传变化在改变的蛋白质功能和视网膜细胞的氧化还原状态之间建立了联系，形成了代谢记忆的状态。尽管各种生化途径是 DR 发病机制的基础，但对视网膜的主要损伤是由于氧化应激，这是改变生化途径的一个统一因素。本综述主要关注 DR 中改变的关键生化途径导致的血管功能障碍，并讨论抗氧化剂作为合理的治疗策略。
