Abstract
Changes in the hemodynamic environment (e.g., hypertension, disturbed-flow conditions) are known to promote atherogenesis by inducing proinflammatory phenotypic alterations in endothelial and smooth muscle cells; however, the mechanisms underlying mechanosensitive induction of inflammatory gene expression are not completely understood. Bone morphogenetic protein-2 and -4 (BMP-2/4) are TGF-β superfamily cytokines that are expressed by both endothelial and smooth muscle cells and regulate a number of cellular processes involved in atherogenesis, including vascular calcification and endothelial activation. This review considers how hemodynamic forces regulate BMP-2/4 expression and explores the role of mechanosensitive generation of reactive oxygen species by NAD(P)H oxidases in the control of BMP signaling. Antioxid. Redox Signal. 11, 1683–1697.
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