Liu Sixuan, Liu Jiachen, Wang Yinhuai, Deng Fei, Deng Zebin
Department of Urology The Second Xiangya Hospital of Central South University Changsha Hunan China.
Xiangya School of Medicine Central South University Changsha Hunan China.
MedComm (2020). 2025 Jul 1;6(7):e70268. doi: 10.1002/mco2.70268. eCollection 2025 Jul.
The dysregulated accumulation of reactive oxygen species (ROS) and reactive nitrogen species disrupts redox homeostasis, triggering oxidative stress (OS) and driving pathophysiological changes across multiple organ systems. OS modulates critical signaling pathways, induces inflammation, impairs mitochondrial function, alters metabolic homeostasis, and dysregulates autophagy, contributing to disease progression. While prior research has largely focused on OS within single-organ diseases (e.g., neurodegenerative, cardiovascular, and oncological disorders), the systemic role of OS in pan-organ diseases and interorgan communication remains insufficiently explored. This review integrates multidisciplinary evidence to elucidate the biological functions of OS in cellular signaling, homeostasis, and cross-organ crosstalk. It systematically dissects OS-driven molecular mechanisms and pathophysiological networks across 10 major organ systems, including the nervous, cardiovascular, oncological, hepatic, and renal systems. Furthermore, it critically examines OS-related therapeutic targets, including antioxidant and ROS-generating enzymes, and explores synergistic redox-based therapeutic strategies. By moving beyond traditional single-organ paradigms, this review constructs a holistic framework to decode the systemic impact of OS, offering novel insights into disease mechanisms and therapeutic innovations. Ultimately, it lays the foundation for precision medicine approaches aimed at mitigating OS-driven diseases and improving multiorgan health outcomes.
活性氧(ROS)和活性氮的积累失调会破坏氧化还原稳态,引发氧化应激(OS),并推动多个器官系统发生病理生理变化。OS调节关键信号通路,诱导炎症,损害线粒体功能,改变代谢稳态,并失调自噬,从而促进疾病进展。虽然先前的研究主要集中在单一器官疾病(如神经退行性疾病、心血管疾病和肿瘤疾病)中的OS,但OS在泛器官疾病和器官间通讯中的系统作用仍未得到充分探索。本综述整合多学科证据,以阐明OS在细胞信号传导、稳态和跨器官串扰中的生物学功能。它系统地剖析了OS驱动的分子机制和横跨10个主要器官系统(包括神经、心血管、肿瘤、肝脏和肾脏系统)的病理生理网络。此外,它还严格审查了与OS相关的治疗靶点,包括抗氧化剂和ROS生成酶,并探索基于氧化还原的协同治疗策略。通过超越传统的单一器官范式,本综述构建了一个整体框架来解读OS的系统影响,为疾病机制和治疗创新提供了新的见解。最终,它为旨在减轻OS驱动的疾病和改善多器官健康结果的精准医学方法奠定了基础。