Michael A. Matthay

This study compares molecular features of SSc-NSIP and SSc-UIP with IPF, finding shared epithelial changes and distinct fibroblast programs.

This study shows that SARS-CoV-2's ORF8 protein reprograms macrophages to enhance viral infection of lung epithelial cells, contributing to lung pathology in COVID-19.

This study identifies age-related epigenetic changes in AT2 cells that promote basal cell metaplasia, contributing to idiopathic pulmonary fibrosis.

This study identifies white adipose tissue lipolysis and circulating fatty acids as key mediators of metabolic tolerance to infection, showing improved survival in sepsis with beta3-adrenergic agonists.

This study investigates how pirfenidone and nintedanib affect the growth and differentiation of human alveolar type 2 cells in organoid cultures, revealing differences in their impact on surfactant protein C expression and cell identity.

This study shows that a fiber-rich diet alters alveolar macrophage metabolism and lung injury responses via gut microbiome-derived propionate.

The paper identifies MMP1high basal cells derived from alveolar type II cells that contribute to microcyst formation in IPF, suggesting a therapeutic target through MMP inhibition or WNT modulation.

This study identifies Mac1 as a therapeutic target for SARS-CoV-2 and demonstrates that AVI-4206, a small molecule inhibitor, reduces viral replication and improves survival in an animal model.

This study shows that fibroblast proliferation drives pulmonary fibrosis and that targeting this process could be a new therapeutic strategy.

This study shows gut bacteria produce lactate that increases lung epithelial mitochondrial activity and worsens acute lung injury.

The paper identifies molecular and structural changes in aging human lungs that contribute to fibrosis and impair lung function.

This paper develops a metagenomic sequencing approach to diagnose lower respiratory tract infections by integrating pathogen detection, microbiome analysis, and host transcriptome data.