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Galectin‐3 (Gal‐3) plays a critical role in vascular inflammation and fibrosis. The role of TGF‐β1 in mediating pulmonary vascular fibrosis is well documented; thus, we suspected that Gal‐3 could be an important factor in TGF‐β1‐induced fibrosis in pulmonary adventitial fibroblasts (PAFs). We treated rats with monocrotaline (MCT) and cultured PAFs with TGF‐β1 to stimulate fibrosis. We found that MCT injection induced vessel thickening and extracellular matrix deposition in vivo. TGF‐β1 stimulated the production of collagen and fibronectin (Fn) protein in vitro. TGF‐β1 promoted the expression of Gal‐3 and its translocation, while silencing Gal‐3 reduced Col‐1a deposition. Blockage of STAT3 decreased the expression of Gal‐3 induced by TGF‐β1. Gal‐3 increased Col‐1a accumulation and downregulated matrix metallopeptidase 9 (MMP‐9) expression in PAFs, but it did not affect Fn expression. These findings demonstrate that Gal‐3 is required for TGF‐β1‐stimulated vascular fibrosis via a STAT3 signaling cascade and that MMP‐9 is also involved in TGF‐β1/Gal‐3‐induced vascular fibrosis.