自噬/巨噬作为一种溶酶体依赖的分解细胞内蛋白质和细胞器的噬菌体途径。自噬功能障碍与许多疾病相关，包括溶酶体贮积病、癌症、神经退行性疾病、心肌病和慢性代谢性疾病，其中还观察到增加的反应性氧化物（ROS）水平。ROS可以随机氧化蛋白质，脂质和DNA，引起氧化应激和损伤。细胞已经发展出各种抗氧化途径以减少过多的ROS并维持红氧稳态。仅针对自噬功能障碍和氧化应激的一方面进行治疗显示出非常有限的效果。因此，识别能够调节自噬和抗氧化途径的桥接因子对双重靶点疗法有益。本综述意在提供关于目前已识别出的连接自噬和Nrf2抗氧化途径的桥接因子以及它们彼此之间的紧密联系的见解。这些因子可能成为同时治疗自噬功能障碍和氧化应激相关疾病的潜在双重目标。版权所有©2023年中国科学技术大学。

Macroautophagy/autophagy is a lysosome-dependent catabolic pathway for the degradation of intracellular proteins and organelles. Autophagy dysfunction is related to many diseases, including lysosomal storage diseases, cancer, neurodegenerative diseases, cardiomyopathy, and chronic metabolic diseases, in which increased reactive oxygen species (ROS) levels are also observed. ROS can randomly oxidize proteins, lipids, and DNA, causing oxidative stress and damage. Cells have developed various antioxidant pathways to reduce excessive ROS and maintain redox homeostasis. Treatment targeting only one aspect of diseases with autophagy dysfunction and oxidative stress shows very limited effects. Herein, identifying the bridging factors that can regulate both autophagy and antioxidant pathways is beneficial for dual-target therapies. This review intends to provide insights into the current identified bridging factors that connect autophagy and Nrf2 antioxidant pathway, as well as their tight interconnection with each other. These factors could be potential dual-purpose targets for the treatment of diseases implicated in both autophagy dysfunction and oxidative stress.Copyright © 2023 Ning, Hang, Zhang, Mao and Li.