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Redox Control of Vascular Smooth Muscle Migration

Journal

ANTIOXIDANTS & REDOX SIGNALING
Volume 12, Issue 5, Pages 625-640

Publisher

MARY ANN LIEBERT, INC
DOI: 10.1089/ars.2009.2852

Keywords

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Funding

  1. National Institutes of Health [HL38206, HL093115, HL058863]
  2. NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [K99HL093115, R01HL038206, R29HL038206, R01HL058863, R00HL093115, R37HL038206] Funding Source: NIH RePORTER

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Vascular smooth muscle cell migration is important during vascular development and contributes to lesion formation in the adult vasculature. The mechanisms regulating migration of this cell type are therefore of great interest. Recent work has shown that reactive oxygen species (ROS) derived from NADPH oxidases are important mediators of promigratory signaling pathways. ROS regulate the intracellular signals responsible for lamellipodia formation, actin cytoskeleton remodeling, focal adhesion turnover, and contraction of the cell body. In addition, they contribute to matrix remodeling, a critical step to initiate and support vascular smooth muscle cell motility. Despite these recent advances in our understanding of the redox mechanisms that contribute to migration, additional work is needed to evaluate fully the potential of ROS-sensitive molecular signals as therapeutic targets to prevent inappropriate smooth muscle cell migration. Antioxid. Redox Signal. 12, 625-640.

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