MiR-214 inhibits apoptosis in thyroid epithelial follicular cells induced by amiodarone through the FASL/MAPK pathway

BackgroundHashimoto's thyroiditis (HT), also known as chronic lymphocytic thyroiditis, is one of the most common autoimmune disease (AITD) in clinical practice. It is urgent to explore the mechanism of amiodarone-induced thyroid dysfunction.ObjectiveThis study aims to assess the expression levels of miR-214 and FasL in amiodarone contact type of HT, and the effect of miR-214 on cell viability and apoptosis and potential mechanism.ResultsWe found that miR-214 was low expressed in the tissues of amiodarone-treated thyroiditis patients. MiR-214 increased the survival rate of amiodarone-induced thyroid epithelial follicular cells and inhibited apoptosis. Mechanically, we found that miR-214 could bind to FASL and regulate MAPK signaling pathway through FASL.ConclusionsOur results suggested that miR-214 could be a potential therapeutic target for Hashimoto's thyroiditis.