Quanyi Zhao

This paper develops an in vitro system that mimics osteochondrogenic differentiation of smooth muscle cells and intimal vascular calcification, showing distinct transcriptional states compared to standard calcification assays.

The paper characterizes atherosclerosis trajectories in vascular smooth muscle cells using single-cell data and identifies causal transcriptomic and epigenomic mechanisms of CAD risk.

This study creates a transcriptomic and spatial atlas of human arterial segments, revealing cell-type and segment-specific heterogeneity linked to vascular disease risk.

The paper links ADAR1-mediated RNA editing in smooth muscle cells to regulation of MDA5 activation, showing its role in atherosclerosis progression and vascular calcification.

This study shows chronic e-cigarette exposure accelerates atherosclerosis by reprogramming smooth muscle cells toward a chondrogenic phenotype through GRIN2A-dependent NMDAR signaling.

The paper identifies causal genetic mechanisms at CAD GWAS loci using CRISPR screens and chromatin analysis, revealing enhancer-gene links and ancestry/sex-specific risk factors.

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 shows dioxin exposure accelerates atherosclerosis by promoting inflammatory smooth muscle cell phenotypes and oxidative stress, with AHR in SMC providing protective effects.

The paper identifies vascular site-specific epigenomic and transcriptomic features and links them to disease risk loci using single-cell data and GWAS integration.

The paper maps QTLs for TCF21 binding, chromatin accessibility, and chromosomal looping in coronary artery smooth muscle cells and links them to CAD GWAS loci.

The paper investigates the role of AHR in atherosclerosis by showing it suppresses chondrogenic fate of modulated smooth muscle cells in lesions.

The paper identifies noncoding RNAs as key mediators linking coronary artery disease GWAS variants to causal genes.