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It is produced in part by degradation of C-mannosylated proteins through the autophagic pathway in cells and is considered a product of protein C-mannosylation turnover ( Beyond metabolic and oxidative stress pathways, our findings also implicate the neuroimmune interface in RA
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Longitudinal studies should be conducted to further assess the potential impact of mitochondrial dysfunction on RA and periodontitis
Geneva: World Health Organization (1969)
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