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doi: 10.2174/138920308785132677
[PubMed 4182379] 135
Mitochondrial dysfunction can contribute to mitochondrial DNA (mtDNA) mutations, increased mitochondrial reactive oxygen species (mtROS), and oxidative stress, which have been progressively underscored in the pathogenesis of RA over recent years (9)
To better understand the efficacy and safety of cell replacement therapy, a variety of experimental models of PD have been established
TSIs mimic the action of TSH by binding to TSHR on follicular epithelial cells, leading to the overstimulation of thyroid hormone production and secretion [14-16]
