Mitochondrial and metabolic dysfunction of peripheral immune cells in multiple sclerosis

• Published in: Journal of neuroinflammation Vol. 21; no. 1; pp. 28 - 19
• Main Authors: Wang, Peng-Fei, Jiang, Fei, Zeng, Qiu-Ming, Yin, Wei-Fan, Hu, Yue-Zi, Li, Qiao, Hu, Zhao-Lan
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 20.01.2024; BioMed Central; BMC
• Subjects: Analysis; Antigens; Apoptosis; Care and treatment; Chemokines; Cytokines; Cytology; Cytotoxicity; Demyelination; Diagnosis; Immune cells; Immune response; Immune system; Immune-metabolic; Inflammation; Lymphocytes; Magnetic resonance imaging; Metabolism; Mitochondria; Mitochondrial DNA; Mitochondrion; Multiple sclerosis; Nerves; Neurodegeneration; Pathogenesis; Phosphorylation; Proteins; T cell receptors; Therapeutic targets; Tumor necrosis factor-TNF; China; Mitochondrion; Immune-metabolic; Immune cells; MS
• ISSN: 1742-2094; 1742-2094
• DOI: 10.1186/s12974-024-03016-8

Multiple sclerosis (MS) is a chronic autoimmune disorder characterized by the infiltration of inflammatory cells and demyelination of nerves. Mitochondrial dysfunction has been implicated in the pathogenesis of MS, as studies have shown abnormalities in mitochondrial activities, metabolism, mitochondrial DNA (mtDNA) levels, and mitochondrial morphology in immune cells of individuals with MS. The presence of mitochondrial dysfunctions in immune cells contributes to immunological dysregulation and neurodegeneration in MS. This review provided a comprehensive overview of mitochondrial dysfunction in immune cells associated with MS, focusing on the potential consequences of mitochondrial metabolic reprogramming on immune function. Current challenges and future directions in the field of immune-metabolic MS and its potential as a therapeutic target were also discussed.