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Idiopathic pulmonary fibrosis (IPF) is a life-threatening and progressive interstitial lung disease. Healthy pulmonary tissues were replaced by an altered extracellular matrix (ECM) and destroyed the alveolar architecture, which led to the disruption of gas exchange, decreased lung compliance, and ultimately led to the failure of respiration and death. IPF is associated with dyspnoea and cough, eventually impairing the quality of a large population worldwide, with the incidence rate increasing drastically with age. The IPF involves a complex pathophysiology; thus, it is necessary to understand the precise molecular mechanism for lung fibrosis to develop novel therapeutic options. Different kinases, including p38 mitogen-activated protein kinase, JNK (c-Jun N-terminal kinase), and SAPKs (Stress-activated protein kinases), were ubiquitously expressed in numerous variety of cells and were activated in response to …