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Muscle atrophy is defined as the progressive degeneration or shrinkage of myocytes and is triggered by factors such as aging, cancer, injury, inflammation, and immobilization. Considering the total amount of body iron stores and its crucial role in skeletal muscle, myocytes may have their own iron regulation mechanism. Although the detrimental effects of iron overload or iron deficiency on muscle function have been studied, the molecular mechanism of iron-dependent muscle atrophy has not been elucidated. Using human muscle tissues and in the mouse rotator cuff tear model, we confirmed an association between injury-induced iron depletion in myocytes and muscle atrophy. In differentiated C2C12 myotubes, the effects of iron deficiency on myocytes and the molecular mechanism of muscle atrophy by iron deficiency were evaluated. Our study revealed that the lower iron concentration in injured muscle was associated with the upregulation of ferroportin, an iron exporter that transports iron out of cells. Ferroportin expression was increased by hypoxia-inducible factor 1α (HIF1α), which is activated by muscle injury, and its expression is controlled by HIF1 inhibitor treatment. Iron deprivation caused myocyte loss and a marked depletion of mitochondrial membrane potential leading to muscle atrophy, together with increased levels of myostatin, the upstream regulator of atrogin1 and muscle RING-finger protein-1 (MuRF1). Myostatin expression under iron deficiency was mediated by an orphan nuclear receptor, dosage-sensitive sex reversal-adrenal hypoplasia congenita critical region on the X chromosome (DAX1).

Background: Post-laminectomy syndrome is a common cause of dissatisfaction after endoscopic interlaminar approach. Our aim was to evaluate the efficacy and safety of our two newly designed instruments for laminotomy, a dural protector attached to the scope and a knot pusher for water-tight suturing of the incidental dural tears. Material and Methods: This was a multicenter evaluation. Efficacy was quantified as the pre-to-postoperative improvement in pain (visual analog scale), disability (Oswestry Disability Index), patient satisfaction (modified MacNab score), and length of hospital stay. Safety was quantified by the incidence and location of dural tears, rate of revision, and radiological outcomes. Outcomes were evaluated between the control (before instrument development) and experimental (after instrument development) groups. Results: There was a significant improvement in leg pain in the experimental group (p = 0.03), with greater patient satisfaction in the control group (p < 0.01). There was no incidence of dural tears in the area of the traversing and exiting nerve roots in the experimental group. Water-tightness of sutures was confirmed radiologically. Conclusion: The novel dural protector and the knot pusher for water-tight sutures improved the efficacy and safety of decompression and discectomy; however, a prolonged operative time was a drawback.