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视网膜色素变性中的氧化还原状态。

Redox Status in Retinitis Pigmentosa.

机构信息

Pathophysiology and Therapies for Vision Disorders, Principe Felipe Research Center (CIPF), Valencia, Spain.

Joint Unit on Rare Diseases CIPF-La Fe, Valencia, Spain.

出版信息

Adv Exp Med Biol. 2023;1415:443-448. doi: 10.1007/978-3-031-27681-1_65.

Abstract

Retinitis pigmentosa (RP) is the most common form of inherited retinal dystrophy characterized by the progressive loss of vision. It is a rare disease. Despite being a genetic disease, its progression is influenced by oxidative damage and chemokines and cytokines released by the activated immune cells (e.g., macrophages or microglia). The role of oxidative stress is very important in the retina. Rods are the main consumers of oxygen (O), so they are constantly exposed to oxidative stress and lipid peroxidation. According to the oxidative hypothesis, after rod death in the early stages of the disease, O would accumulate in large quantities in the retina, producing hyperoxia and favoring the accumulation of reactive oxygen species and reactive nitrogen species that would cause oxidative damage to lipids, proteins, and DNA, exacerbating the process of retinal degeneration. Evidence shows alterations in the antioxidant-oxidant state in patients and in animal models of RP. In recent years, therapeutic approaches aimed at reducing oxidative stress have emerged as useful therapies to slow down the progression of RP. We focus this review on oxidative stress and its relationship with the progression of RP.

摘要

色素性视网膜炎(RP)是最常见的遗传性视网膜营养不良,其特征是视力逐渐丧失。它是一种罕见的疾病。尽管它是一种遗传性疾病,但它的进展受到氧化损伤和由激活的免疫细胞(如巨噬细胞或小胶质细胞)释放的趋化因子和细胞因子的影响。氧化应激在视网膜中起着非常重要的作用。视杆细胞是氧气(O)的主要消耗者,因此它们不断受到氧化应激和脂质过氧化的影响。根据氧化假说,在疾病早期视杆细胞死亡后,大量的 O 在视网膜中积累,产生过氧,并有利于活性氧和活性氮的积累,从而导致脂质、蛋白质和 DNA 的氧化损伤,加剧视网膜变性过程。证据表明,患者和 RP 动物模型中的抗氧化剂-氧化剂状态发生了改变。近年来,旨在降低氧化应激的治疗方法已成为减缓 RP 进展的有用疗法。我们专注于氧化应激及其与 RP 进展的关系。

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