Hanjoong Jo

This study identifies desert hedgehog (DHH) as a resilience factor that prevents atherosclerosis by inhibiting PAI-1 signaling and endothelial mesenchymal transition.

This paper identifies immunomodulatory endothelial cells (IMEC) that present antigens on MHC class II and activate T cells in atherosclerosis.

This study identifies HEG1 as a flow-sensitive protein that regulates eNOS activity, preventing endothelial dysfunction, hypertension, and atherosclerosis.

This study identifies FAK activity as a mediator of disturbed flow-induced atherosclerosis through the VEGFR2-Cbl-NF-κB signaling pathway in endothelial cells.

This study validates the two-hit hypothesis showing disturbed flow and hypercholesterolemia together reprogram endothelial cells to immune-like and foam cells during atherogenesis.

This study shows that endothelial CTR1 senses disturbed flow by increasing mitochondrial copper, leading to cuproptosis and atherosclerosis, and identifies a therapeutic target.

The paper describes the development of a corrected Poldip2 floxed mouse model, identifies a mutation in initial models, and characterizes the effects of Poldip2 knockout in mice.