Journal
ANTIOXIDANTS & REDOX SIGNALING
Volume 11, Issue 7, Pages 1683-1697Publisher
MARY ANN LIEBERT, INC
DOI: 10.1089/ars.2008.2401
Keywords
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Funding
- American Heart Association [0430108N, 0435140N]
- National Institutes of Health [HL077256, HL-43023]
- American Diabetes Association
- Philip Morris U.S A.
- Philip Morris International, Inc.
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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. Antioxid. Redox Signal. 11, 1683-1697.
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