Juyong Brian Kim

TL;DR: A protective role for both TCF21 and SMC phenotypic modulation in this disease is established and these cells transform into unique fibroblast-like cells, termed ‘fibromyocytes’, rather than into a classical macrophage phenotype.

TL;DR: This study assessed the effect of transtricuspid placement of permanent pacemaker (PPM) and implantable cardioverter defibrillator (ICD) leads on tricuspid regurgitation (TR) in 248 patients with echocardiograms before and after placement.

TL;DR: This work uses integrative genomic, epigenomic and transcriptomic profiling of perturbed human coronary artery smooth muscle cells and tissues to begin to identify causal regulatory variation and mechanisms responsible for CAD associations, and validates the findings in expression quantitative trait loci cohorts.

TL;DR: Genome wide RNA-Seq studies in human coronary artery SMC with siRNA knockdown suggest that TCF21 may have a role regulating the differentiation state of SMC precursor cells that migrate into vascular lesions and contribute to the fibrous cap and provide evidence that these processes may be a mechanism for CAD risk attributable to the vascular wall.

TL;DR: These data indicate that TCF21 antagonizes the MYOCD-SRF pathway through multiple mechanisms, further establishing a role for this coronary artery disease-associated gene in fundamental SMC processes and indicating the importance of smooth muscle response to vascular stress and phenotypic modulation of this cell type in coronary arteries disease risk.