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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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Mechanistic investigations associate these outcomes with signaling pathways involving vascular endothelial growth factor receptor-2 (VEGFR-2) and downstream Akt-eNOS activation, processes that collectively facilitate efficient muscle tissue remodeling (5)