We showed that iodine-induced autophagy suppression facilitates the induction of apoptosis by activating ROS, which is regulated by the downregulation of TGF-β1 in TFCs.
Decreased autophagy and enhanced apoptosis levels were observed in the thyroid tissues of HT patients, thus suggesting that excess iodine may initiate HT development by inhibiting autophagy and promotion of apoptosis in TFCs.
Therefore, optimization of iodine intake is an important component of preventive health care aiming to reduce the prevalence of thyroid disorders.