Postoperative stability reconstruction following spinal tumor resection is a critical step to ensure functional recovery and quality of life for patients. This article systematically reviews the current status of anterior and posterior column reconstruction techniques after spinal tumor resection, including strategies such as bone cement augmentation, structural implants, and three-dimensional-printed personalized prostheses. It emphasizes the need for individualized treatment plans based on tumor type, anatomical location, and the patient’s overall condition. The article also highlights the importance of restoring sagittal balance, multidisciplinary collaboration, and complication prevention for long-term outcomes. In the future, innovations in biomaterials, along with the minimally invasive and intelligent evolution of surgical techniques, will further advance the goal of achieving stable, pain-free, and functionally effective spinal reconstruction for each patient, ultimately enhancing their quality of life.
With the oxidative damage model established in rat myocardial cells by hydrogen peroxide (H2O2), the expression of myocardin and nuclear factor erythroid 2-related factor 2 (Nrf2) during oxidative damage and effect of myocardin on Nrf2 were preliminarily explored. The expression of the target gene was increased or decreased by transfection of plasmid DNA or shRNA, respectively. Cell proliferation was detected by sulforhodamine B (SRB) assay. The expression of myocardin mRNA and Nrf2 mRNA was detected by Real-time PCR, and their protein levels were detected by Western blot. The results showed that oxidative damage was induced by H2O2 with an optimized incubation condition of 200 μmol/L H2O2 for 24 hours. H2O2 inhibited expression of myocardin in mRNA and protein levels, and increased expression of Nrf2 in mRNA and protein levels. The overexpression of myocardin or the knockdown of Nrf2 significantly decreased cell viability compared with the control group, while the knockdown of myocardin or the overexpression of Nrf2 significantly increased cell viability. The overexpression of myocardin significantly down-regulated the expression of Nrf2 in mRNA and protein levels, while the knockdown of myocardin dramatically up-regulated the expression of Nrf2. Thus, it is deduced that myocardin may inhibit cell proliferation and Nrf2 may promote cell proliferation. Oxidative damage induced by H2O2 in rat myocardial cell might activate Nrf2-related signaling pathway through down-regulation of myocardin.
