WNT3A and pulmonary fibrosis: In lung fibroblasts, either primary or immortalized Mlg lines, it suppressed nuclear accumulation of β-catenin and promoted its phosphorylation and degradation concomitant with loss of Wnt3a-induced LRP6 phosphorylation, with similar effects observed in vivo, exerting preventive effects in a bleomycin-induced mouse model of pulmonary fibrosis [23].