State Key Laboratory for Animal Disease Control and Prevention, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin 150069, China.
Agricultural College, Yanbian University, Yanji 133002, China.
Int J Mol Sci. 2024 Aug 24;25(17):9206. doi: 10.3390/ijms25179206.
Mitochondria play pivotal roles in sustaining various biological functions including energy metabolism, cellular signaling transduction, and innate immune responses. Viruses exploit cellular metabolic synthesis to facilitate viral replication, potentially disrupting mitochondrial functions and subsequently eliciting a cascade of proinflammatory responses in host cells. Additionally, the disruption of mitochondrial membranes is involved in immune regulation. During viral infections, mitochondria orchestrate innate immune responses through the generation of reactive oxygen species (ROS) and the release of mitochondrial DNA, which serves as an effective defense mechanism against virus invasion. The targeting of mitochondrial damage may represent a novel approach to antiviral intervention. This review summarizes the regulatory mechanism underlying proinflammatory response induced by mitochondrial damage during viral infections, providing new insights for antiviral strategies.
线粒体在维持各种生物功能中发挥着关键作用，包括能量代谢、细胞信号转导和固有免疫反应。病毒利用细胞代谢合成来促进病毒复制，可能破坏线粒体功能，并随后在宿主细胞中引发一连串的促炎反应。此外，线粒体膜的破坏参与免疫调节。在病毒感染过程中，线粒体通过生成活性氧（ROS）和释放线粒体 DNA 来协调固有免疫反应，线粒体 DNA 作为一种有效的防御机制来对抗病毒入侵。靶向线粒体损伤可能是一种新的抗病毒干预方法。本综述总结了病毒感染过程中线粒体损伤诱导促炎反应的调控机制，为抗病毒策略提供了新的见解。
