Emerging roles of NLRP3 inflammasome-mediated pathways in pulmonary fibrosis: Current knowledge and therapeutic strategies.

Pulmonary fibrosis (PF) is a highly disabling and fatal chronic lung disease with limited treatment options. Chronic inflammation is considered a crucial pathological mechanism underlying the initiation and progression of PF. The NLRP3 inflammasome plays a significant role in this process, primarily by activating and releasing a cascade of proinflammatory mediators through interactions with various signaling pathways. Mechanistically, in the pulmonary microenvironment, the NLRP3 inflammasome triggers a robust inflammatory response via pathogen-associated molecular patterns (PAMPs), which leads to alveolar epithelial cell (AEC) damage and promotes the differentiation of fibroblasts into myofibroblasts. These pathological processes contribute to excessive deposition of extracellular matrix (ECM) components, driving fibrotic remodeling. In this review, we present the biological functions of the NLRP3 inflammasome in PF and delve into the specific mechanisms by which NLRP3-related pathways regulate PF progression. Furthermore, we explore the latest research on modulating NLRP3 inflammasome activation as a potential therapeutic strategy for PF, emphasizing the therapeutic potential of NLRP3-related pathways as targets for anti-fibrotic treatment.