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The information from the included articles was listed by publication date to provide chronological order (Table 1)

We identified genes and pathways as candidate therapeutic targets for HF and provided the basis for follow-up experiments to evaluate the potential of these genes and pathways in the treatment of HF

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TGF- directly elevates transcription of collagen genes (COL1A1, COL3A1) via the Smad pathway and induces additional pro-fibrotic mediators (CTGF, PDGF, FGF), synergistically promoting fibroblast proliferation and collagen synthesis ( EMT not only directly damages alveolar architecture but its heterogeneity is closely associated with clinical differences among disease subtypes