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![Overview of pathogenesis and
pathophysiological progression in pulmonary fibrosis. The schematic
illustrates the multi-layered interactions-including genetic
predisposition, environmental exposures, age-related decline and
immune dysregulation - that collectively drive disease initiation.
The interplay of these factors triggers a sequential pathogenic
cascade beginning with alveolar epithelial cell injury, followed by
dysregulated inflammation and immune activation, leading to
fibroblast recruitment and myofibroblast differentiation and
culminating in excessive extracellular matrix deposition and tissue
remodeling. ROS, reactive oxygen species; 1-NP, 1-nitropyrene; BaP,
benzo[a]pyrene; MUC5B, mucin 5B, oligomeric mucus/gel-forming;
TERT, telomerase reverse transcriptase; TERC, telomerase RNA
component; rs35705950, a single nucleotide polymorphism in the
MUC5B promoter region; TOLLIP, toll interacting protein.](/article_images/ijmm/57/5/ijmm-57-05-05783-g00.jpg)
