TWEAK/Fn14 axis in respiratory diseases

被引:21
|
作者
Wang, Min [1 ]
Xie, Zhijuan [2 ]
Xu, Jin [3 ]
Feng, Zhuyu [4 ]
机构
[1] Univ South China, Dept Otorhinolaryngol, Affiliated Nanhua Hosp, Hengyang 421002, Peoples R China
[2] Univ South China, Dept Nephrol, Affiliated Hosp 1, Hengyang 421001, Peoples R China
[3] Changsha Med Univ, Sch Pharmaceut Sci, Changsha 410219, Hunan, Peoples R China
[4] Univ South China, Dept Crit Care Med, Affiliated Nanhua Hosp, Hengyang 421002, Peoples R China
关键词
Respiratory diseases; TWEAK; Fn14; NF-KAPPA-B; OBSTRUCTIVE SLEEP-APNEA; SKELETAL-MUSCLE ATROPHY; INDUCIBLE FACTOR-I; LUNG-CANCER CELLS; WEAK INDUCER; APOPTOSIS TWEAK; RECEPTOR FN14; MULTIFUNCTIONAL CYTOKINE; FUNCTIONAL EXPRESSION;
D O I
10.1016/j.cca.2020.06.007
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is a well known multifunctional cytokine extensively distributed in cell types and tissues. Accumulating evidence has shown that TWEAK binding to the receptor factor-inducible 14 (Fn14) participates in diverse pathologic processes including cell proliferation and death, angiogenesis, carcinogenesis and inflammation. Interestingly, alterations of intracellular signaling cascades are correlated to the development of respiratory disease. Recently, a several lines of evidence suggests that TWEAK in lung tissues are closely associated with these signaling pathways. In this review, we explore if TWEAK could provide a novel therapeutic strategy for managing respiratory disease in general and pulmonary arterial hypertension (PAH), obstructive sleep apnea syndrome (OSAS), asthma, idiopathic pulmonary fibrosis (IPF), chronic obstructive pulmonary disease (COPD) and non-small cell lung cancer (NSCLC), specifically.
引用
收藏
页码:139 / 148
页数:10
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