Department of Physiology, New York Medical College, Valhalla, New York, USA.
Antioxid Redox Signal. 2009 Jul;11(7):1683-97. doi: 10.1089/ars.2008.2401.
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-beta 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.
血流动力学环境的变化(例如高血压、血流紊乱等)已知可通过诱导内皮细胞和平滑肌细胞的促炎表型改变来促进动脉粥样硬化形成;然而,机械敏感诱导炎症基因表达的机制尚不完全清楚。骨形态发生蛋白 2 和 4(BMP-2/4)是 TGF-β超家族细胞因子,内皮细胞和平滑肌细胞均可表达,并调节动脉粥样硬化形成过程中涉及的许多细胞过程,包括血管钙化和内皮细胞激活。本综述考虑了血流动力学如何调节 BMP-2/4 的表达,并探讨了 NAD(P)H 氧化酶产生的机械敏感活性氧在控制 BMP 信号中的作用。