These results align with CDN’s established anti-fibrotic roles in fibrosis [20,21], yet they reveal a distinct mechanism of action in pulmonary fibrosis: whereas CDN ameliorates liver and kidney fibrosis primarily via suppressing TGF-β or NF-κB cascades, its anti-fibrotic effect in BLM-induced alveolar epithelial injury appears to be mediated predominantly through the inhibition of IGF1/PI3K/AKT signaling [21]. This evidence concerns the gene IGF1 and pulmonary fibrosis.