AI Article Synopsis
- Myofibroblast apoptosis resistance contributes to the progression of pulmonary fibrosis (PF), particularly in idiopathic pulmonary fibrosis (IPF) cases.
- Researchers discovered that mesenchyme homeobox 1 (MEOX1) is overexpressed in lung tissues of IPF patients and in mouse models with PF.
- Silencing MEOX1 reduces PF severity and increases myofibroblast apoptosis by targeting the G-protein signaling pathway regulator RGS4, suggesting that MEOX1 could be a potential therapeutic target for PF treatment.
Article Abstract
The apoptosis resistance of myofibroblasts is a hallmark in the irreversible progression of pulmonary fibrosis (PF). While the underlying molecular mechanism remains elusive. In this study, we unveiled a previously unrecognized mechanism underlying myofibroblast apoptosis resistance during PF. Our investigation revealed heightened expression of mesenchyme homeobox 1 (MEOX1) in the lungs of idiopathic pulmonary fibrosis (IPF) patients and bleomycin-induced PF mice. Silencing MEOX1 significantly attenuated PF progression in mice. In vitro, we found a notable increase in MEOX1 expression in transforming growth factor-β1 (TGF-β1)-induced myofibroblasts. Silencing MEOX1 enhanced apoptosis of myofibroblasts. Mechanistically, we identified G-protein signaling pathway regulatory factor 4 (RGS4) as a critical downstream target of MEOX1, as predicted by bioinformatics analysis. MEOX1 enhanced apoptosis resistance by upregulating RGS4 expression in myofibroblasts. In conclusion, our study highlights MEOX1 as a promising therapeutic target for protecting against PF by modulating myofibroblast apoptosis resistance.
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| http://dx.doi.org/10.1002/jcp.31442 | DOI Listing |
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