Simon R. Johnson

This study identifies three novel genetic signals associated with idiopathic pulmonary fibrosis using GWAS and clinically-curated datasets, highlighting potential drug targets like MUC1 and NTN4.

This study identifies extracellular matrix genes that reduce rapamycin response in LAM cells and suggests repurposed inhibitors as potential therapies.

This study shows mTOR dysregulation in LAM causes IL6 production and senescence in AT2 cells, impairing lung repair, and suggests targeting IL6 may help.

The paper uses spatial multiomic profiling to identify distinct fibrotic epithelial niches in IPF, revealing a KRT5low/KRT17 epithelial population and its association with SPP1 macrophages.

The paper identifies rare pathogenic variants associated with pulmonary fibrosis by analyzing whole genome sequencing data and linking them to cytoskeletal dysfunction.

This study investigates the association between mosaic loss of chromosome Y (mLOY) and pulmonary fibrosis, finding mLOY correlates with age and telomere length but not disease severity, and suggests a potential link between telomere shortening and mLOY.

A stabilized miR-29 mimic, MRG-229, shows efficacy at lower doses and good safety in preclinical models, supporting its development for pulmonary fibrosis.