Jeffrey Craig Horowitz

The paper identifies distinct peripheral PUFA metabolites associated with different causes and severity of ARDS, suggesting potential biomarkers and therapeutic targets.

The paper identifies SorlA as a novel PAI-1 interactor required for lung fibrosis, showing SorlA deficiency protects against fibrosis in mice and SorlA is upregulated in human IPF lung tissue.

This study examines how glycosylation mutations in the NTD of the SARS-CoV-2 XEC variant affect neutralizing antibody responses, cell-cell fusion, and spike stability.

This study evaluates neutralization, infectivity, and stability of JN.1-derived SARS-CoV-2 subvariants, finding that DelS31 mutation in the NTD reduces nAb titers, impairs infectivity, and increases spike stability.

This study evaluates neutralization resistance, infectivity, and membrane fusion of JN.1-derived SARS-CoV-2 subvariants SLip, FLiRT, and KP.2, identifying key mutations affecting antibody sensitivity and spike function.

This study compares immune evasion, antigenicity, and cell-cell fusion properties of SARS-CoV-2 BA.2.87.1 and JN.1 variants, finding BA.2.87.1 shows less neutralization escape and higher infectivity than JN.1 and XBB.1.5.

This study compares immune evasion, infectivity, and fusogenicity of SARS-CoV-2 variants BA.2.86 and FLip using neutralization assays and cell-based experiments.

This study identifies endothelial TLR3 insufficiency as a mechanism underlying SARS-CoV-2-induced lung vascular remodeling and suggests TLR3 agonists as a potential therapeutic strategy.