Abstract
Caldesmon is a negative regulator of cell proliferation, migration, and metalloproteinase release. Caldesmon function is regulated by multiple kinases, targeting multiple phosphorylation sites. Recently, overexpression of caldesmon has been shown to inhibit neointimal formation after experimental angioplasty, suggesting that caldesmon may be a potential therapeutic target for proliferative vascular diseases.
Keywords: Actin, atherosclerosis, caldesmon, calmodulin, restenosis, vascular smooth muscle
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