These results suggest that the significant activation of TGF-β1/Smad3 signaling pathway in lung tissues after CHF can lead to myofibroblast proliferation and a marked upregulation of type I collagen expression, suggesting that QL could suppress the TGF-β1/Smad3 signaling pathway, which might contribute to its attenuation of lung fibrosis in CHF. Here, SMAD3 is linked to congestive heart failure.