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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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JNK involves in effector T cells function by stimulating Th1 differentiation in RA synovial tissue (131)

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