YKL-40 通过激活 FAK 和 MAPK 信号通路介导哮喘中的气道重塑。
YKL-40 mediates airway remodeling in asthma via activating FAK and MAPK signaling pathway.
机构信息
Insititute of Burn Surgery, Changhai Hospital, Second Military Medical University , Shanghai, China.
Department of Respiratory and Critical Care Medicine, Changzheng Hospital, Second Military Medical University , Shanghai, China.
出版信息
Cell Cycle. 2020 Jun;19(11):1378-1390. doi: 10.1080/15384101.2020.1750811. Epub 2020 Apr 14.
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-40 . and . 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.
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。哮喘中的气道重塑涉及复杂的生理和病理过程，包括由于增殖、气道平滑肌细胞迁移、上皮-间充质转化（EMT）和上皮下纤维化导致的气道平滑肌质量增加。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。在这项研究中，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 通路可以显著改善 YKL-40 过度分泌引起的气道重塑。总之，这项研究阐明了 YKL-40 在哮喘气道重塑中的作用，并为 YKL-40 水平较高的哮喘患者提供了潜在的新靶点。
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