Multiple sclerosis (MS) is characterized by chronic,slowly expanding lesions with the accumulation of myeloid cells,which lead to brain atrophy and progressive disability.The role of mitochondria,especially mitochondr...Multiple sclerosis (MS) is characterized by chronic,slowly expanding lesions with the accumulation of myeloid cells,which lead to brain atrophy and progressive disability.The role of mitochondria,especially mitochondrial respiratory complexes and metabolites,in controlling myeloid immune responses,is well-documented but not fully understood in diseases of the central nervous system (CNS).The groundbreaking study by Prof.Peruzzotti-Jametti et al.[1],entitled"Mitochondrial complexⅠactivity in microglia sustains neuroinflammation"published in Nature,delves into the intricate dynamics between mitochondrial function within microglia and the perpetuation of chronic neuroinflammation,specifically in MS.The core point of their investigation is the hypothesis that mitochondrial complexⅠ(CI) activity,through a mechanism known as reverse electron transport (RET),generates reactive oxygen species (ROS) in microglia,thereby sustaining inflammatory response in the CNS.This increases ROS production from the mitochondria,which is thought to be a crucial factor in the maintenance of a pro-inflammatory state in the microglia,contributing to the pathology of MS and similar neuroinflammatory diseases.展开更多
基金supported by the Taishan Scholars Program of Shandong Province(tsqn202312344).
文摘Multiple sclerosis (MS) is characterized by chronic,slowly expanding lesions with the accumulation of myeloid cells,which lead to brain atrophy and progressive disability.The role of mitochondria,especially mitochondrial respiratory complexes and metabolites,in controlling myeloid immune responses,is well-documented but not fully understood in diseases of the central nervous system (CNS).The groundbreaking study by Prof.Peruzzotti-Jametti et al.[1],entitled"Mitochondrial complexⅠactivity in microglia sustains neuroinflammation"published in Nature,delves into the intricate dynamics between mitochondrial function within microglia and the perpetuation of chronic neuroinflammation,specifically in MS.The core point of their investigation is the hypothesis that mitochondrial complexⅠ(CI) activity,through a mechanism known as reverse electron transport (RET),generates reactive oxygen species (ROS) in microglia,thereby sustaining inflammatory response in the CNS.This increases ROS production from the mitochondria,which is thought to be a crucial factor in the maintenance of a pro-inflammatory state in the microglia,contributing to the pathology of MS and similar neuroinflammatory diseases.
