Systemic lupus erythematosus(SLE),a chronic autoimmune disease,is marked by impaired immune tolerance and heightened activity in both innate and adaptive immune systems.Hallmarks of SLE include elevated type I interfe...Systemic lupus erythematosus(SLE),a chronic autoimmune disease,is marked by impaired immune tolerance and heightened activity in both innate and adaptive immune systems.Hallmarks of SLE include elevated type I interferons and autoantibody production,though the exact causes of SLE remain elusive despite advances in research techniques.Crucial to SLE research is understanding its pathogenesis and developing effective diagnostic and therapeutic methods.Recent studies have highlighted a significant link between mitochondrial abnormalities and SLE's development and progression.Mitochondrial dysfunction plays a key role in SLE pathogenesis through various mechanisms such as mitochondrial DNA mutations,oxidative stress,immune metabolic reprogramming,and cellular death.These factors collectively contribute to the loss of self-tolerance,increased autoantibody production,and impaired clearance of immune complexes,leading to their deposition.This triggers sustained inflammatory responses and damages multiple organs.This review focuses on the diagnostic and therapeutic approaches related to mitochondrial abnormalities in SLE.Targeting mitochondrial pathways presents a promising strategy for treating SLE,potentially improving prognosis and quality of life for those affected.Future research should further investigate the role of mitochondria in the onset and progression of SLE,providing new avenues for understanding and managing this complex disease.展开更多
基金Key Research and Development Program of Jiangxi Municipal Science and Technology Department,Grant/Award Number:20192BBGL70024Science and Technology Program of Department of Health of Jiangxi Province,Grant/Award Number:20204254National Key Research and Development Program of China,Grant/Award Number:2021YFC2501304。
文摘Systemic lupus erythematosus(SLE),a chronic autoimmune disease,is marked by impaired immune tolerance and heightened activity in both innate and adaptive immune systems.Hallmarks of SLE include elevated type I interferons and autoantibody production,though the exact causes of SLE remain elusive despite advances in research techniques.Crucial to SLE research is understanding its pathogenesis and developing effective diagnostic and therapeutic methods.Recent studies have highlighted a significant link between mitochondrial abnormalities and SLE's development and progression.Mitochondrial dysfunction plays a key role in SLE pathogenesis through various mechanisms such as mitochondrial DNA mutations,oxidative stress,immune metabolic reprogramming,and cellular death.These factors collectively contribute to the loss of self-tolerance,increased autoantibody production,and impaired clearance of immune complexes,leading to their deposition.This triggers sustained inflammatory responses and damages multiple organs.This review focuses on the diagnostic and therapeutic approaches related to mitochondrial abnormalities in SLE.Targeting mitochondrial pathways presents a promising strategy for treating SLE,potentially improving prognosis and quality of life for those affected.Future research should further investigate the role of mitochondria in the onset and progression of SLE,providing new avenues for understanding and managing this complex disease.
