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Glycolysis and Autoimmune Diseases: A Growing Relationship

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Biochemistry (Moscow), Supplement Series A: Membrane and Cell Biology Aims and scope

Abstract

Under homeostasis states, proliferation, differentiation and function of immune cells are efficiently regulated to not only support the protection against pathogens, but also to prevent the autoimmune attack against self-tissues. It is now authenticated that immune cell activation is engaged with intense alterations in cellular metabolism. Accumulating body of data indicated that alterations in the metabolism of immune cells have a tight association with the pathogenesis of autoimmune diseases. Aerobic glycolysis is a major element in activation and differentiation of T cells. It has been established that aerobic glycolysis plays an essential role in the various pathophysiological aspects of several autoimmune diseases. A new emerging field of the specialty “Immunometabolism” has been developed and holds promise to explore new therapeutic targets. With consideration of common profile of metabolic perturbation in autoimmune diseases, targeting of these metabolic dysregulation heralds a beginning of a new chapter in the treatment of autoimmune diseases. In this review, we set out to discuss how glycolysis pathway can affect autoreactive T-cell differentiation/functions and also describe the latest findings associated with glucose metabolism and autoimmune diseases. Finally, we introduce new therapeutic approaches that could potentially alter metabolic perturbation and correct the Th17/Treg imbalance in autoimmune diseases.

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ACKNOWLEDGMENTS

We would like to apologize to all our colleagues whose important work could not be cited directly. Contribution: R-R., design and manuscript writing; S.-T., manuscript writing; D.A., final approval of manuscript; M.R.-A., research and table design.

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Abbreviations: AMPK, 5' AMP-activated protein kinase; CIA, collagen-induced arthritis; CNS, central nervous system; CSF, cerebrospinal fluid; DC, dendritic cell; DCA, dichloroacetate; 2DG, 2-deoxy-D-glucose; FADD, Fas-associated protein with death domain; EAE, experimental autoimmune encephalomyelitis; ECAR, extracellular acidification rate; eIF4E, eukaryotic translation initiation factor 4E; ERK, extracellular signal-related kinase; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; GBS, Guillain-Barré syndrome; GlcNAc, amino sugar N-acetylglucosamine; HIF-1, hypoxia-inducible factor 1; IBD, inflammatory bowel disease; IKK-NF-kappaB, IkappaB kinase-nuclear factor kappaB; iNOS, inducible nitric oxide synthase; IPF, idiopathic pulmonary fibrosis; LDH, lactate dehydrogenase; LXR, liver X receptor; MRS, magnetic resonance spectroscopy; MS, multiple sclerosis; mTOR, mammalian target of rapamycin; NOX, nicotinamide dinucleotide phosphate oxidase; NOXO, nicotinamide dinucleotide phosphate oxidase organizer I; OCR, oxygen consumption rate; PPARγ, peroxisome proliferator-activated receptor gamma; RA, rheumatoid arthritis; SLE, systemic lupus erythematosus; SSc, systemic sclerosis; STAT5, signal transducer and activator of transcription 5; T1D, type 1 diabetes; TC, trans-chromosomic; TCR, T-cell receptor; Th, T helper cells; TPI, triose phosphate isomerase; Treg, regulatory T cells.

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Rezaei, R., Tahmasebi, S., Atashzar, M.R. et al. Glycolysis and Autoimmune Diseases: A Growing Relationship. Biochem. Moscow Suppl. Ser. A 14, 91–106 (2020). https://doi.org/10.1134/S1990747820020154

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