dynamic changes of smooth muscle cells in multi-omics during atherogenesis

Robust evidence supports the concept that vascular SMC "plasticity", "de-differentiation" and "phenotype switching" are key determinants of atherogenesis and lesional destabilization. While few studies have investigated the upstream regulators of phenotype switching and SMC diversity. Here, we applied a combination of whole-genome sequencing, whole transcriptome sequencing, single-cell transcriptomic profiling, and single-cell chromatin accessibility technology to address these questions in lineage-traced SMCs isolated from a mouse model of atherosclerosis.