Iain D. Stewart

This study identifies a monocyte-macrophage-fibroblast axis in post-COVID-19 lung fibrosis using multi-omic profiling and shows its potential as a therapeutic target.

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 performs GWAS of IPF using dominant and recessive models, identifying five new genome-wide significant signals and genes, including PMF1 and EPN3, and observing increased PMF1 expression in IPF patients.

This study shows that an AKAP13 genetic variant promotes fibrosis by altering epithelial signaling, and inhibiting AKAP13's RhoGEF activity reduces fibrotic markers in IPF models.

This study identifies SLC15A4 as a susceptibility gene for IPF through genome-wide analysis of tandem repeat variation, showing its role in gene expression and disease risk.

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.

This paper investigates how galectin-3 enhances TGF-β1 activation and signaling in lung fibroblasts, contributing to idiopathic pulmonary fibrosis.

This study identifies four genetic loci, including one novel, with shared causal variants between severe COVID-19 and idiopathic pulmonary fibrosis (IPF), revealing both shared and distinct biological processes.