Skeletal muscle has a remarkable regeneration capacity to recover its structure and function after injury, except for the traumatic loss of critical muscle volume, called volumetric muscle loss (VML). Although many extremity VML models have been conducted, craniofacial VML has not been well-studied due to unavailable in vivo assay tools. Here, this paper reports a wireless, noninvasive nanomembrane system that integrates skin-wearable printed sensors and electronics for real-time, continuous monitoring of VML on craniofacial muscles. The craniofacial VML model, using biopsy punch-induced masseter muscle injury, shows impaired muscle regeneration. To measure the electrophysiology of small and round masseter muscles of active mice during mastication, a wearable nanomembrane system with stretchable graphene sensors that can be laminated to the skin over target muscles is utilized. The noninvasive system provides highly sensitive electromyogram detection on masseter muscles with or without VML injury. Furthermore, it is demonstrated that the wireless sensor can monitor the recovery after transplantation surgery for craniofacial VML. Overall, the presented study shows the enormous potential of the masseter muscle VML injury model and wearable assay tool for the mechanism study and the therapeutic development of craniofacial VML.

Oculopharyngeal muscular dystrophy (OPMD) is a late-onset dominant disease that primarily affects craniofacial muscles. Despite the fact that the genetic cause of OPMD is known to be expansion mutations in the gene encoding the nuclear polyadenosine RNA binding protein PABPN1, the molecular mechanisms of pathology are unknown and no pharmacologic treatments are available. Due to the limited availability of patient tissues, several animal models have been employed to study the pathology of OPMD. However, none of these models have demonstrated functional deficits in the muscles of the pharynx, which are predominantly affected by OPMD. Here, we used a knock-in mouse model of OPMD, Pabpn1+/A17, that closely genocopies patients. In Pabpn1+/A17 mice, we detected impaired pharyngeal muscle function, and impaired pharyngeal satellite cell proliferation and fusion. Molecular studies revealed that basal autophagy, which is required for normal satellite cell function, is higher in pharynx-derived myoblasts than in myoblasts derived from limb muscles. Interestingly, basal autophagy is impaired in cells derived from Pabpn1+/A17 mice. Pabpn1 knockdown in pharyngeal myoblasts failed to recapitulate the autophagy defect detected in Pabpn1+/A17 myoblasts suggesting that loss of PABPN1 function does not contribute to the basal autophagy defect. Taken together, these studies provide the first evidence for pharyngeal muscle and satellite cell pathology in a mouse model of OPMD and suggest that aberrant gain of PABPN1 function contributes to the craniofacial pathology in OPMD.

Nanomembrane Electronics In article number 2101037 by Woon‐Hong Yeo, Hyojung J. Choo, and co‐workers, a wireless, non‐invasive nanomembrane system is reported that integrates wearable printed electronics for real‐time, continuous monitoring of volumetric muscle loss (VML) on craniofacial muscles. The craniofacial VML model, using biopsy punch‐induced masseter muscle injury, shows impaired muscle regeneration.

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