强直性脊柱炎炎性骨破坏和病理性骨化的信号转导机制

The mechanism of signal transduction of inflammatory cytokines and pathological bone formation in ankylosing spondylitis

炎性骨破坏和病理性骨化是强直性脊柱炎的特征性病理表现,有多种细胞因子和信号通路参与其中。目前,肿瘤坏死因子а、白细胞介素是最广为人知的参与炎性破坏的细胞因子,与此同时,伴随着越来越多新的生物学标志物的出现,Wnt/β-catenin信号通路、BMP/TGF-β信号通路等在AS骨化中的作用也日益受到重视。细胞因子介导的炎症与病理性骨化信号通路之间关系的研究,可能从分子水平上揭示强直性脊柱炎从炎症到骨化过程的机制,并为TNF抑制剂的长期临床应用提供依据。

The pathological features of ankylosing spondylitis （AS） include inflammatory bone destruction and ectopic bone formation. Variety of cytokines and signaling pathways are involved in these two processes. At present, tumor necrosis factor-a and interleukins are most well-known inflammatory cytokines which lead to bone damage. Meanwhile, appearing of many new biomarkers, such as Wnt/β-catenin signaling pathway and BMP/TGF-β signaling pathway, are attracting more and more attention. The study of the relationship between cytokines and signal pathways may reveal the mechanism of inflammation and pathological ossification in AS, which provides the evidence for the long-term use of anti-TNF drugs.