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Background Multiple sclerosis (MS) is a major global problem, and as its pathogenesis is understood more clearly, therapeutic options expand accordingly. The mitochondrial open reading frame of the 12S rRNA-c (MOTS-c) is a novel mitochondria-derived protein acting on metabolic homeostasis. In this study, we aimed to investigate the role of serum MOTS-c in the pathophysiology of the disease in MS patients and to discuss the mechanism of MOTS-c.

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