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Abstract Purpose To explore the effect of sarcopenia on recurrent fractures of adjacent vertebra after percutaneous kyphoplasty (PKP). Methods A total of 376 osteoporotic vertebral compression fractures (OVCFs) patients over 55 years old who were admitted to the Hospital from August 2020 to January 2021 were selected. Among them, 38 patients with recurrent fractures in adjacent vertebra after PKP were selected as the refracture group (RG), and the remaining 338 patients were selected as the non-refracture group (NRG). The age, gender, grip strength, body mass index (BMI), bone mineral density (BMD), visual analogue scale (VAS) of pain before and one month after surgery, Oswestry disability index (ODI) before and one month after surgery and the occurrence of sarcopenia were compared between the two groups. Logistic regression analysis was used to evaluate the effect of related risk factors on refracture after vertebral PKP. Results The results of t-test and Chi-square test showed that there were no obvious differences in gender, BMI, preoperative VAS score (t=-0.996, P = 0.320) and ODI (t=-0.424, P = 0.671), one month postoperative VAS score (t=-0.934, P = 0.355) and ODI score (t=-0.461, P = 0.645). while the age and grip strength showed significant differences between the two groups. Logistic regression analysis showed that BMI and gender had no significant effect on refracture after PKP, while sarcopenia and advanced age were independent risk factors for refracture after PKP. Also, increased BMD was a protective factor for refracture after PKP. Conclusion Sarcopenia is an independent risk factor for recurrent fractures after PKP in OVCF patients. The screening and diagnosis of sarcopenia should be strengthened. At the same time, anti-sarcopenia treatment should be actively performed after surgery.

NUAK2 is a member of the AMP-activated protein kinase (AMPK) family, which plays an essential role in cellular processes such as apoptosis, proliferation, and cell fate. Recent studies have already shown that silencing of NUAK2 blocks proliferation and promotes apoptosis of human melanoma cells and liver cancer cells. In addition, NUAK2 is involved in the development of glioblastoma via regulating the expression of cancer stem cell-related genes, and it promotes the cell cycle entry in the glioblastoma cells. However, the expression and the role of NUAK2 in the progress of peripheral nerve regeneration after injury are yet to be elucidated. We observed that NUAK2 was upregulated following distal sciatic nerve crush (SNC). Interestingly, we discovered that NUAK2 showed co-localization with S100 (Schwann cell marker). Furthermore, we found that the NUAK2 had a spatiotemporal protein expression, which was consistent with proliferating cell nuclear-antigen (PCNA). The protein level of NUAK2 and YAP was upregulated in the model of TNF-α-induced Schwann cell (SC) proliferation. Furthermore, flow cytometry analysis, CCK-8, transwell assays, and wound healing assays were all performed with the purpose of exploring the role of NUAK2 in the regulation of SC proliferation and migration. More importantly, we found that NUAK2-deficient SCs showed significantly reduced expression of Yes-associated protein (YAP). Bioinformatic analysis identified upstream regulators of NUAK2 and NUAK2-associated genes (e.g., YAP1). Finally, we investigated the recovery changes during regeneration progress through the walking track analysis. Thus, we speculated that NUAK2 was involved in biochemical and physiological responses of SCs after SNC via YAP-driven proliferation and migration, and this study determined the importance of NUAK2 as a potential target in peripheral nerve regeneration.