Exploring the potential regulation of DUOX in thyroid hormone‑autophagy signaling via IGF‑1 in the skeletal muscle (Review).

Abstract

Dual oxidases (DUOX) are enzymes that have the main function in producing reactive oxygen species (ROS) in various tissues. DUOX also play an important role in the synthesis of H₂O₂, which is essential for the production of thyroid hormone. Thyroid hormones can influence the process of muscle development through direct stimulation of ROS, 5' AMP-activated protein kinase (AMPK) and mTOR and indirect effect autophagy and the insulin-like growth factor 1 (IGF-1) pathway. IGF-1 signaling controls autophagy in two ways: Inhibiting autophagy through activation of the PI3K/AKT/mTOR/MAPK pathway and promoting mitophagy through the nuclear factor erythroid 2-related factor 2-binding receptor Bcl2/adenovirus E1B 19 kDa protein-interacting protein 3. Thyroid hormone deficiency caused by the absence of DUOX should be considered because it might have a significant effect on the growth of skeletal muscle. The effect of DUOX regulation on thyroid hormone autophagy via IGF-1 in skeletal muscle has not been well investigated. The present review discussed the regulatory interactions between DUOX, thyroid hormone, IGF-1 and autophagy, which can influence skeletal muscle development.