Basic research on mechanism of lumbar disc degeneration and ne w development of treatment

ERa/GRIP 1与TGF -B/MKK 6/p38 MAPK通路的相互作用通过调节细胞外基质的表达而对软骨代谢起保护作用; PHD 3通过调节NF-κB信号而调控TNF-α的活性。当PHD 3沉默时，TNF -α诱导的分解代谢标志物（包括ADAMTS 5、syndecan 4、MMP 13）表达显著降低，同时聚集蛋白聚糖和II型胶原表达恢复。在体内研究中，退行性腰椎侧凸的Cobb角和CPII之间存在显著的正相关性。结果表明，退行性腰椎侧凸患者有较高水平的II型胶原蛋白的合成和降解。这些发现可能会导致一种新的治疗方法的发展软骨退变

Crosstalks between ERa/GRIP1 and TGF -b/MKK6/p38 MAPK pathway have protective roles on cartilage metabolism via regulating the extracellular matrices expression.PHD3 controls TNF-α activity by modulating NF-κB signaling. When PHD3 is silenced, there is a significant decrease in TNF -α-induced expression of catabolic markers that include ADAMTS5, syndecan4, MMP13, and at the same time, there is restoration of aggrecan and collagen type II expression. In vivo study, there was a significant positive correlation between the Cobb angle and CPII in degenerative lumbar scoliosis. The results suggest degenerative lumbar scoliosis patients have higher levels of type II collagen synthesis and degradation. These findings may lead to the development of a novel therapeutic approach for cartilage degeneration