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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

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This was meant to allow more reliable measurement of LPO parameters such as ethane and pentane exhalation