Chang Jie Mick Lee

Single-cell and spatial maps of human coronary arteries identify FAP as a marker of SMC-derived modulated cells; an anti-FAP BiTE reduced plaque burden in mouse models.

The paper shows that CTCF loss in mouse heart cells reorganizes enhancer activity-by-contact scores, reduces CRH numbers, increases CRH size, and increases CRH crossing TAD boundaries.

The paper identifies cell-type-specific enhancer-gene interactions in cardiac cells and maps disease-associated SNPs to enhancers in endothelial cells.

This study identifies RUNX1 as a key regulator of cardiac recovery by reprogramming macrophages, showing that its inhibition promotes heart function recovery in a chronic heart failure model.

The paper identifies macrophage-like vascular smooth muscle cells as dominant in early atherosclerosis and shows that targeting iron regulation inhibits their transition.

This paper links CAD GWAS variants to causal genes in SMCs using single-cell chromatin accessibility and Hi-C data, creating a scV2E2G map for disease mechanism discovery.

This study identifies BNIP-2 as a key organizer of focal adhesion nanostructure that enhances signaling and traction force, essential for cardiomyocyte differentiation.

This study shows that loss of CTCF in mouse cardiomyocytes disrupts gene neighbourhoods, leading to ectopic enhancer-promoter interactions and heart failure.

The paper identifies genetic variants associated with heart failure by analyzing histone acetylation QTLs in human heart tissue.