Article
Leiomodin 1 haploinsufficiency promotes smooth muscle cell proliferation and increases neointimal lesion size.
Vascular pharmacology - 1 Dec 2025
Wennersten Sara A, Wang Hongxia, Franklin J Lee, Nanda Vivek
Abstract excerpt
The transition of smooth muscle cells (SMCs) from a contractile to a synthetic phenotype is a key contributor to cardiovascular disease (CVD) pathologies, such as atherosclerosis and in-stent restenosis. We previously reported that loss of leiomodin 1 (LMOD1), a coronary artery disease risk gene highly expressed in SMCs, promotes SMC phenotypic switching in vitro. However, the in vivo role of LMOD1 and the...
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