Fig. 1: LNP-mRNA treatment for pulmonary fibrosis and relevant mechanisms.

Overactivated fibroblasts induce pulmonary fibrosis and increase ECM stiffness, which hinders AT2 to AT1 differentiation resulting in PATS accumulation and fibrosis progression. Transient FAPCAR-T cells generated in vivo via LNP-mRNA can eliminate overactivated fibroblasts and promote lung regeneration via alveolar epithelial polarization. (BLM: bleomycin; LNP: lipid nanoparticle; ECM: extracellular matrix; AT1/2: alveolar epithelial type I/II; PATS: pre-alveolar type I transitional cell state). Created in BioRender65.