Platycodin D2 Targets Vimentin to Suppress Fibroblast-Myofibroblast Transition: A Novel Therapeutic Strategy Against Pulmonary Fibrosis

Platycodin D2 binds vimentin with Kd = 392.8 nM and suppresses fibroblast-to-myofibroblast transition and bleomycin-induced pulmonary fibrosis in vivo.

• Why it matters: Pulmonary fibrosis progresses with excessive extracellular matrix deposition and limited effective targets, and vimentin-linked fibroblast activation is a promising but underexploited drug focus.
• What they did: The study screened novel vimentin ligands by virtual screening, confirmed binding by SPR, assessed structural effects with CETSA and CD spectroscopy, and tested antifibrotic activity in vitro and in a bleomycin-induced mouse model.
• The result: PD2 altered vimentin secondary structure and induced insoluble aggregation, inhibited TGF-{beta}1-induced FMT in vitro, mitigated collagen deposition in vivo, and mutagenesis identified Glu138 (chain A), Glu132 and Glu143 (chain B), and Glu50 and Arg54 (chain C) as essential interaction residues.

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