ArticleCirculation research2025
CEMIP Maintains Vascular Contractility by Controlling PP1c-MLC20 Cascade in SMCs.
Article in Circulation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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9 authors.
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Abstract
backgroundThe CEMIP (cell migration-inducing protein) exhibits extremely high expression levels in smooth muscle tissues. However, whether CEMIP modulates the contractile phenotype of vascular smooth muscle cells and confers blood pressure remains elusive.
methodsTo explore the role of CEMIP in SMCs, we generated a mouse model with SMC-specific CEMIP deficiency (SMC-
resultsCEMIP is abundantly expressed in smooth muscle tissues including the mesenteric artery, aorta, and intestine. In a serum-starved contractile phenotype, SMCs responded to serum stimulation by gradually decreasing CEMIP expression, as they shifted to a secretory phenotype. The mice lacking CEMIP in SMCs showed significantly reduced contractility and blood pressure compared with their counterparts of age-matched wild-type littermates (
conclusionsCEMIP functions as a gatekeeper for maintaining the contractile phenotype of SMCs via the PP1c-MLC20 cascade. CEMIP is indispensable for maintaining blood pressure.
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