巨噬细胞极化
牙周炎
PI3K/AKT/mTOR通路
蛋白激酶B
炎症
癌症研究
M2巨噬细胞
巨噬细胞
信号转导
化学
医学
免疫学
细胞生物学
生物
内科学
体外
生物化学
作者
Hailin Mu,Beining Yang,Yan Wang,Shuo Wang,Wenqian Yu,Meie Jia,Wei Dong,Xinyi Wang,Xiaoxiao Xu,Zhipeng Dong,Baochen Yang,X. Li,Jiawei Wang
摘要
Disruption in the collaboration between extracellular matrix (ECM) and immune system is a significant pathology in periodontitis. Macrophages are a crucial part of the immune system and have unique functions, such as polarization. Fibulin-3, an ECM protein, may play a vital role in this dynamic interplay. Fibulin-3 expression is elevated in periodontitis and is closely related to immune cell function. Inhibiting fibulin-3 can alleviate periodontitis by reducing infiltration of immune cells and M1 macrophage ratio. Furthermore, fibulin-3 promoted macrophage M1 polarization by activating the PI3K/AKT signaling pathway through EGFR binding. Our findings offer a clinically relevant rationale for immune response modulation through fibulin-3.
科研通智能强力驱动
Strongly Powered by AbleSci AI