Jeffrey E. Saffitz

This study shows that PAI-1 deficiency leads to early cardiac hemorrhage and fibrosis under hemodynamic stress, with mutations in the protease-inhibitory domain causing similar pathology.

This study shows that Angiotensin II exacerbates mitral valve and left atrial pathology in Fbn1C1041G/+ mice, while AGT inhibition does not alter the phenotype.

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

This study determines the structural basis of Cx45 gating and Ca2+ regulation using cryo-EM, revealing a dual steric-electrostatic mechanism.

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 uses computational models to show that low levels of PKP2 gene therapy transduction in ACM patients do not significantly improve conduction velocity but may increase conduction block risk with higher transduction.

This study shows that inhibiting soluble epoxide hydrolase reduces inflammation and myocardial injury in arrhythmogenic cardiomyopathy by increasing pro-resolving lipid mediators.