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作 者:周岐原 李京宴 田英平[1] 姚咏明[2] Zhou Qiyuan;Li Jingyan;Tian Yingping;Yao Yongming(Emergency Department,The Second Hospital of Hebei Medical University,Shijiazhuang 050000,Hebei,China;Translational Medicine Research Center,Medical Innovation Research Division of the Chinese People's Liberation Army General Hospital,Beijing 100853,China)
机构地区:[1]河北医科大学第二医院急诊医学科,河北石家庄050000 [2]解放军总医院医学创新研究部转化医学研究中心,北京100853
出 处:《生物医学转化》2024年第4期13-21,36,共10页Biomedical Transformation
基 金:国家自然科学基金重点项目(82241062);国家自然科学基金青年科学基金项目(82302412);河北省自然科学基金项目(H2023206202);北京市自然科学基金项目(7244296)。
摘 要:脓毒症是宿主对感染反应失调所致致命性器官功能障碍,其发展与金属元素代谢异常和线粒体质量受损密切相关。线粒体作为能量代谢及金属储存中心,其质量控制参与调控金属介导的细胞死亡,并影响脓毒症发生发展过程。本文将从线粒体质量控制机制及其与金属诱导细胞死亡之间的关系展开综述,探讨脓毒症状态下机体金属代谢与线粒体质量控制变化对细胞死亡的影响,阐明二者相互作用在脓毒症及相关并发症的病理生理过程中的重要性,为脓毒症的诊疗提供新思路。Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection.Its progression is closely associated with metal metabolism abnormalities and mitochondrial quality deterioration.Mitochondria serve as centers for energy metabolism and metal storage,and their quality control regulates metal-mediated cell death,influencing the progression of sepsis.This review discusses the mechanisms of mitochondrial quality control(MQC) and their relationship with metal-induced cell death.It explores the effects of metal metabolism and MQC changes on cell death under septic conditions.The interaction between these factors is further examined for its significance in the pathophysiological processes of sepsis and related complications.This paper provides new insights for its diagnosis and treatment.
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