Emily A. Shiel

This study shows that blocking CD14 reduces arrhythmogenic cardiomyopathy in mice by decreasing inflammation and fibrosis.

Human arrhythmogenic cardiomyopathy hearts harbor a lesion niche of POSTN fibroblasts and NLRP3+ inflammatory macrophages; IL-1β neutralization in Dsg2-mutant mice reduced fibrosis, dysfunction, and ventricular ectopy.

This study shows that PAD4-dependent NETosis and MPO contribute to inflammation, fibrosis, and arrhythmias in ACM, with targeting these pathways improving cardiac function.

This study shows that DSG2 deficiency causes cardiac dysfunction by impairing Z-disc and intercalated disc mechanotransduction, leading to structural and functional cardiac defects.

This paper describes a directed protein evolution method to enhance the catalytic efficiency of CRISPR-Cas9 variants, showing up to 4-fold improvement in AceCas9 and 2-fold increase in HDR-based gene insertion for SpyCas9.