Introduction
Pulmonary fibrosis (PF) is a chronic fibrotic interstitial lung disease characterized by progressive dyspnea and declining lung function. While pirfenidone and nintedanib have been approved for PF treatment, demonstrating efficacy in improving lung function and slowing disease progression during clinical trials, they are associated with adverse effects and tolerability issues. Furthermore, the underlying pathomechanisms of PF remain insufficiently understood(1-3).
The incomplete understanding of PF and the lack of safe and effective therapies have emerged as significant challenges in recent years. As a result, extensive research has been conducted in this field using various in vitro and in vivo models to investigate PF(4). In vitro models enable intricate investigations within cellular and tissue contexts, playing a crucial role in comprehending the pathogenic mechanisms of PF at the cellular and molecular levels(5). Processes such as cellular communication, metabolic activities, and signal transduction mechanisms are central to the pathogenesis of PF(6). At present, researchers commonly utilize PF patients, experimental murine models, genetically modified mouse strains, and in vitro-cultured cells to study PF. However, a definitive representative in vitro cell model remains elusive, hindering a comprehensive understanding of PF pathogenesis.
Therefore, the main objective of this review is to present and compare different in vitro cellular models used in the study of PF, as well as to review their application in various mechanistic studies.