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Together, these interconnected signaling cascades reshape transcriptional programs in fibroblasts, AECs, and endothelial cells, promoting myofibroblast differentiation, epithelial cell dysfunction, immune dysregulation, and excessive ECM deposition, which collectively drive the onset and progression of pulmonary fibrosis [33, 39] (Fig
The research also included qualitative assessments of data from case reports, case series, pharmacovigilance analyses, and other studies unsuitable for quantitative pooling
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