Role of microRNA in Oxidative Stress

Stresses Pub Date : 2024-04-09 DOI:10.3390/stresses4020016
Sarmistha Saha
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Abstract

An imbalance between the formation of reactive oxygen species (ROS) and the reaction of antioxidant proteins is referred to as oxidative stress. NFE2L2/Nrf2, also known as nuclear factor erythroid-derived 2-related factor 2, is a critical enabler of cytoprotective responses to oxidative and electrophilic insults. When Nrf2 is activated, it triggers the transcription of numerous cytoprotective genes, whose promoter regions contain antioxidant response elements (AREs). In recent times, the regulation of Nrf2 by miRNAs has garnered significant attention, among the various mechanisms that govern Nrf2 signaling. It has been reported that a number of miRNAs directly suppress the expression of Nrf2s, which in turn negatively regulates the Nrf2-dependent cellular cytoprotective response. Furthermore, it has been shown that Nrf2 itself regulates miRs, which carry out some of Nrf2’s unique metabolic regulation functions. Here, we provide an overview of the functions and mechanisms of action of miRs as downstream effectors of Nrf2, as well as in their regulation of its activity.
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微小核糖核酸在氧化应激中的作用
活性氧(ROS)的形成与抗氧化蛋白的反应之间的不平衡被称为氧化应激。NFE2L2/Nrf2又称核因子红细胞衍生2相关因子2,是对氧化和亲电损伤做出细胞保护反应的关键因素。当 Nrf2 被激活时,它会触发许多细胞保护基因的转录,这些基因的启动子区域含有抗氧化反应元件(AREs)。近来,在支配 Nrf2 信号传导的各种机制中,miRNA 对 Nrf2 的调控引起了人们的极大关注。据报道,一些 miRNAs 直接抑制 Nrf2s 的表达,进而负向调节 Nrf2 依赖性细胞保护反应。此外,研究还表明,Nrf2 本身可调控 miRs,而 miRs 可发挥 Nrf2 的一些独特代谢调控功能。在这里,我们将概述 miRs 作为 Nrf2 下游效应物的功能和作用机制,以及它们对 Nrf2 活性的调控。
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