VCN managed to halt the progression of fibrosis either directly by interfering with the classical TGF-β1/Smad2/3 signaling pathway or indirectly by upregulating the expression of Nrf2, enhancing the antioxidant system, activating PPAR-γ and downregulating the NLRP3/NF-κB pathway which influences the production of inflammatory cytokines involved in the pathogenesis of pulmonary fibrosis. Here, SMAD2 is linked to pulmonary fibrosis.