Research progress of NLRP3 inflammasome in pulmonary fibrosis / 中国职业医学

ABSTRACT

In recent years, the prevalence of pulmonary fibrosis is increasing worldwide. Due to its complex pathogenesis and different clinical manifestations, the treatment options are limited. The nucleotide-binding oligomerization domain like receptor family pyrin domain-containing protein 3(NLRP3) inflammasome plays an important role in pulmonary fibrotic diseases, and its activation and inhibition can directly affect the process of pulmonary fibrosis. The structure of NLRP3 inflammasome consists of a sensor molecule, NLRP3, apoptosis-associated speck-like protein CARD, and caspase-1. There are three signaling pathways that include canonical pathway, selective or noncanonical pathway, and alternative pathway. Excessive activation of NLRP3 inflammasome can accelerate the development of idiopathic pulmonary fibrosis and pulmonary fibrosis induced by silicosis. Therefore, the NLRP3 inflammasome may serve as a therapeutic target of pulmonary fibrosis. NLRP3 inflammasome activators and inhibitors can mediate the activation and inhibition of NLRP3 inflammasome, and then regulate the occurrence and development of pulmonary fibrosis. Inhibiting the activation of NLRP3 inflammasome can improve pulmonary fibrosis. However, the specific mechanism has not been elucidated. The therapeutic strategies for pulmonary fibrosis need further research on the activation and regulation of NLRP3 inflammasome.