David A. Lomas

This study evaluates changes in circulating alpha-1 antitrypsin (AAT) monomers and polymers after liver transplantation in PiZZ AAT deficiency patients.

This study shows that both terminal misfolding and polymerisation of Z 1-antitrypsin contribute to liver disease phenotypes, with terminal misfolding driving pro-fibrotic responses and metabolic changes.

The paper investigates the earliest steps of protein misfolding during alpha-1-antitrypsin biosynthesis, revealing co- and post-translational folding pathways and their implications for disease.

This study expands the genetic landscape of COPD by identifying 82 risk loci, revealing associations with lung function, cell types, and comorbidities.