
Researchers identified the FHL5 gene as the top candidate causal gene at the UFL1-FHL5 locus associated with coronary artery disease/myocardial infarction through fine-mapping and functional analyses. FHL5 regulates smooth muscle cell contraction and promotes vascular calcification under procalcifying conditions. These findings provide mechanistic insights into the pleiotropic genetic associations of UFL1-FHL5 and its role in vascular disease risk.
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