Autophagy's Role in Maxillofacial Muscle Regeneration: A Review

The maxillofacial muscles comprise the masticatory and expression muscles, which receive innervation from the trigeminal and facial nerves, respectively. Although autophagy's role in skeletal muscle regeneration has been extensively studied, limited attention has been given to maxillofacial muscle regeneration. Nevertheless, since both types of muscles are skeletal, it is reasonable to assume that autophagy's involvement in maxillofacial muscle regeneration is similar to that of other skeletal muscles.

In an effort to simulate traditional oral surgery, Seki Y developed a rat trigeminal nerve denervation model, which demonstrated upregulation of Rab24, an autophagy marker involved in autophagosome formation, in the injured trigeminal motor nucleus after surgical denervation. Additionally, in the klotho mouse, a model for aging, masseter and tongue muscle weight and myofiber diameter were significantly decreased, accompanied by activation of the autophagic-lysosomal pathway in the masseter and tongue, to maintain survival activities such as mastication, swallowing, and respiration.

Recent studies have shown that sleep deprivation for 96 hours increased LC3 expression in both masseter and temporal muscles, while over 96 hours, sleep deprivation decreased autophagy levels, as evidenced by decreased LC3. Another study reported that autophagy played an important role in regulating hypoxic stress in genioglossus muscle-derived stem cells (GG MDSCs). Sustained hypoxia promoted the expression of LC3II and Beclin1 in GG MDSCs, as well as the HIF-1α/BNIP3 signaling pathway.

These findings suggest that autophagy plays a crucial role in maintaining normal maxillofacial muscle functions and regeneration. However, overstimulation could reduce autophagy levels, highlighting the need for further investigation.