Open AccessTherapeutic Potential of Janus Kinase Inhibitors for the Management of Interstitial Lung Disease
Author(s) -
Rongxiu Huo,
Qi Guo,
Junping Hu,
Na Li,
Rui Gao,
Liangyu Mi,
Zhaoliang Zhang,
Hechao Liu,
Zhiying Guo,
Haitao Zhao,
Liyun Zhang,
Ke Xu
Publication year - 2022
Publication title -
drug design, development and therapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.964
H-Index - 64
ISSN - 1177-8881
DOI - 10.2147/dddt.s353494
Subject(s) - janus kinase , jak stat signaling pathway , interstitial lung disease , stat protein , stat , pulmonary fibrosis , cancer research , fibrosis , medicine , idiopathic pulmonary fibrosis , inflammation , myofibroblast , janus kinase 2 , stat3 , signal transduction , lung , immunology , biology , pathology , cytokine , receptor , microbiology and biotechnology , tyrosine kinase
Interstitial lung disease (ILD) refers to a heterogeneous group of diseases characterized by lung fibroblast proliferation, interstitial inflammation, and fibrosis-induced lung damage. The Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway is known to be activated by pro-fibrotic/pro-inflammatory cytokines such as IL-6 and IL-13, whose levels are elevated in ILD. The overexpression of growth factors such as transforming growth factor β1 in ILD activates the JAK/STAT pathway through classical or non-classical pathways, promotes macrophage activation, increases the release of pro-inflammatory and pro-fibrosis factors, and facilitates fibroblast differentiation into myofibroblasts. These findings implicate that the JAK/STAT pathway plays an important role in the course of ILD. Recent evidence also suggests that JAK inhibition alleviates excessive inflammation and pulmonary fibrosis. Accordingly, the JAK inhibitors may serve as promising drugs for the treatment of JAK/STAT-induced ILD.