YKL-40 mediates airway remodeling in asthma via activating FAK and MAPK signaling pathway
YKL-40 mediates airway remodeling in asthma via activating FAK and MAPK signaling pathway
复制标题
YKL-40通过激活FAK和MAPK信号通路介导哮喘气道重塑
DOI：
10.1080/15384101.2020.1750811
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发表时间：
2020-04-13
期刊：
影响因子：
4.3
通讯作者：
Tang, Hao
中科院分区：
文献类型：
--
作者：
Sun, Yu;Shi, Zhaoquan;Tang, Hao
YKL-40是一种几丁质酶样蛋白，在哮喘患者中显著升高，与哮喘严重程度和气道重塑密切相关。哮喘气道重塑涉及复杂的生理和病理过程，包括气道平滑肌细胞增殖、迁移、上皮间质转化（EMT）和上皮下纤维化等。然而，YKL-40在这种病理改变中的确切作用和潜在机制仍不清楚。在本研究中，我们证明YKL-40可以通过增加气道平滑肌质量，诱导EMT和上皮下纤维化来促进哮喘气道重塑。此外，我们发现FAK和MAPK信号通路在此过程中被激活。抑制FAK或MAPK通路可显著改善YKL-40过度分泌所致的气道重塑。和体内。本研究为进一步研究YKL-40在哮喘气道重塑中的作用提供了新的靶点。
YKL-40 is a chitinase-like protein which was significantly elevated in asthma patients and related closely to asthma severity and airway remodeling. Airway remodeling in asthma involves complicated physical and pathological processes, including increased airway smooth muscle mass due to proliferation, migration of airway smooth muscle cells, epithelial-mesenchymal transition (EMT) and sub-epithelial fibrosis. However, the precise effect and underlying mechanism of YKL-40 in this pathological alteration remained unelucidated. In this study, we demonstrated that YKL-40 could promote asthma airway remodeling by increasing airway smooth muscle mass, inducing EMT and sub-epithelial fibrosis. Furthermore, we identified that FAK and MAPK signaling pathways are activated in the process. Inhibiting FAK or MAPK pathway could significantly ameliorate airway remodeling induced by excessive secretion of YKL-40in vitro. andin vivo. In conclusion, this study shed light upon the effects of YKL-40 in asthma airway remodeling and provided potential novel targets in asthma patients with high YKL-40 level.