Zhang Zijia, Du Bin, Wu Xunyao, Hu Xiaoyun, Diao Shitong, Dong Run
MICU, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100010, China.
Department of Critical Care Medicine, Peking Union Medical College Hospital, Beijing, 100010, China. Corresponding author: Du Bin, Email:
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2025 Mar;37(3):300-304. doi: 10.3760/cma.j.cn121430-20241126-00957.
Patients with severe pneumonia caused by novel coronavirus infection are often complicated with acute respiratory distress syndrome (ARDS), which has a high mortality. ARDS is characterized by diffuse alveolar damage, pulmonary edema, and hypoxemia. Mitochondria are prone to morphological and functional abnormalities under hypoxia and viral infection, which can lead to cell apoptosis and damage, severely impacting the disease progression. Mitochondria maintain homeostasis through fission and fusion. In ARDS, hypoxia leads to the phosphorylation of dynamin-related protein 1 (Drp1), triggering excessive mitochondrial fission and damaging the alveolar epithelial barrier. Animal experiments have shown that inhibiting this process can alleviate lung injury, providing a potential direction for treatment. The pathology of novel coronavirus infection-related ARDS is similar to that of typical ARDS but more severe. Viral infection and hypoxia disrupt the mitochondrial balance, causing fission and autophagy abnormalities, promoting oxidative stress and mitochondrial DNA (mtDNA) release, activating inflammasomes, inducing the expression of hypoxia-inducible factor-1α (HIF-1α), exacerbating viral infection, inflammation, and coagulation reactions, and resulting in multiple organ damage. Mechanical ventilation and glucocorticoids are commonly used in the treatment of novel coronavirus infection-related ARDS. Mechanical ventilation is likely to cause lung and diaphragm injuries and changes in mitochondrial dynamics, while the lung protective ventilation strategy can reduce the adverse effects. Glucocorticoids can regulate mitochondrial function and immune response and improve the patient's condition through multiple pathways. The mitochondrial dynamics imbalance in novel coronavirus infection-related ARDS is caused by hypoxia and viral proteins, leading to lung and multiple organ injuries. To clarify the pathophysiological mechanism of mitochondrial dynamics imbalance in novel coronavirus infection-related ARDS and explore effective strategies for regulating mitochondrial dynamics balance to treat this disease, so as to provide new treatment targets and methods for patients with novel coronavirus infection-related ARDS. The existing treatments have limitations. Future research needs to deeply study the mechanism of mitochondrial dysfunction, develop new therapies and regulatory strategies, and improve the treatment effect.
新型冠状病毒感染所致重症肺炎患者常并发急性呼吸窘迫综合征（ARDS），其死亡率很高。ARDS的特征为弥漫性肺泡损伤、肺水肿和低氧血症。在缺氧和病毒感染情况下，线粒体易于出现形态和功能异常，这可导致细胞凋亡和损伤，严重影响疾病进展。线粒体通过分裂和融合维持内稳态。在ARDS中，缺氧导致动力相关蛋白1（Drp1）磷酸化，引发过度的线粒体分裂并破坏肺泡上皮屏障。动物实验表明，抑制这一过程可减轻肺损伤，为治疗提供了潜在方向。新型冠状病毒感染相关ARDS的病理与典型ARDS相似，但更严重。病毒感染和缺氧破坏线粒体平衡，导致分裂和自噬异常，促进氧化应激和线粒体DNA（mtDNA）释放，激活炎性小体，诱导缺氧诱导因子-1α（HIF-1α）表达，加剧病毒感染、炎症和凝血反应，导致多器官损伤。机械通气和糖皮质激素常用于新型冠状病毒感染相关ARDS的治疗。机械通气可能导致肺和膈肌损伤以及线粒体动力学改变，而肺保护性通气策略可减少不良反应。糖皮质激素可调节线粒体功能和免疫反应，并通过多种途径改善患者病情。新型冠状病毒感染相关ARDS中线粒体动力学失衡由缺氧和病毒蛋白引起，导致肺和多器官损伤。为阐明新型冠状病毒感染相关ARDS中线粒体动力学失衡的病理生理机制，探索调节线粒体动力学平衡以治疗该疾病的有效策略，从而为新型冠状病毒感染相关ARDS患者提供新的治疗靶点和方法。现有治疗存在局限性。未来研究需要深入研究线粒体功能障碍机制，开发新的治疗方法和调控策略，提高治疗效果。
