Gábor Csányi

This study identifies MEIS1 as an activator of myocardin and vascular smooth muscle cell differentiation, showing its role in promoting the quiescent, differentiated state.

This study shows that loss of Leiomodin1 in vascular smooth muscle cells causes rapid coronary atherosclerosis in mice, independent of actin nucleation, and highlights Thbs1 as a target for mitigating foam cell formation.

This study shows that loss of neurofibromin activates GLUT1 in macrophages, leading to increased glycolysis and retinal neovascularization in NF1 mice.

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