Advances in the study of mitochondrial dysfunction in the pathogenesis of rheumatoid arthritis
LU Yixian
GUO Jinchen
LU Jia
ZHANG Wenjing
WANG Honglei
Abstract：Rheumatoid arthritis(RA)is a chronic systemic autoimmune disease characterized by the hyperplasia of synovial cells,an increase in inflammatory cells,and the destruction of cartilage.The pathogenesis of RA is complex and closely related to genetic factors,immune system abnormalities,and mitochondrial dysfunction.Mitochondria,known as the powerhouse of the cell,play a pivotal role in the development of RA.Their dysfunction is manifested as abnormal energy metabolism,excessive accumulation of reactive oxygen species(ROS),and abnormal activation of the innate immune system,which in turn promotes inflammation and tissue damage.The pathogenic environment of RA influences mitochondrial dysfunction through hypoxic conditions,DNA mutations,and oxidative stress.Hypoxia impairs mitochondrial function,promoting inflammation and angiogenesis;mutations in mitochondrial DNA(mtDNA)exacerbate mitochondrial dysfunction and advance the progression of RA;oxidative stress directly damages cartilage and the extracellular matrix,altering protein structure.Therefore,investigating the relationship between mitochondrial dysfunction and the pathogenesis of RA is of significant importance for understanding the disease's mechanisms and developing novel therapeutic strategies.
Keywords：Rheumatoid arthritisMitochondrial dysfunctionOxidative stressInflammationImmune response
Publication Date：2024-10-01
Online Publishing Date：2025-08-15(First online date of this platform, not the publication date of the document)
Pages：7( 789-795 )