Sara A. Wennersten

Leiomodin 1 deficiency promotes lipid accumulation and redirects gene regulatory programs in smooth muscle cells exposed to oxidized LDL

The transition of smooth muscle cells (SMCs) from a contractile to a synthetic, lipid-accumulating phenotype is a central driver of atherosclerosis. We previously identified leiomodin 1 (LMOD1), an SMC-enriched gene, as a critical regulator of SMC phenotypic modulation and atherosclerosis in mice. However, whether LMOD...