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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

Frontiers in Nutrition, 9 , 874254.

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

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