Fig. 1

Schematic overview of major mechanisms and key regulators in macrophage polarization, fibroblast activation and AEC transformation within PF microenvironment. (IL: interleukin; ECM: extracellular matrix; TGF-β1: transforming growth factor-beta; TNF α: Tumor Necrosis Factor-α; NF κB: nuclear factor kappa-light-chain-enhancer of activated B-cells; NLRP3: NLR Family Pyrin Domain Containing 3; ApoE: apolipoprotein E; LPR1: lipoprotein receptor-related protein 1; TLR: Toll-like receptors; CSF1R: clinically available colony-stimulating factor receptor-1; LPS: lipopolysaccharides; IFN-γ: interferon-γ; MEF2C: myocyte enhancer factor 2 C; STAT6: Signal Transducer And Activator Of Transcription 6; MMP: matrix metalloproteinases; CXCR4: C-X-C receptor 4; CXCL: C-X-C motif ligand; ECM: extracellular matrix; YAP: Yes-Associated Protein; TAZ: Tafazzin; FMT: fibroblast-to-myofibroblast transformation; PI3K: phosphatidylinositol 3-kinase; FAP: fibroblast activation protein; JNK: JUN N -terminal kinases; ECM: extracellular matrix; JNK: JUN N -terminal kinases; WISP-1: WNT1inducible-signaling pathway protein 1; SASP: senescence-associated secretory phenotype; IGF-1: insulin like growth factor 1; JAK/STAT: Janus tyrosine Kinase-Signal Transducer and Activator of Transcription; MFN: mitochondrial fusion proteins mitofusin)