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.