Disturbed-Flow-Mediated Vascular Reactive Oxygen Species Induce Endothelial Dysfunction

DOI Web Site PubMed 被引用文献7件 参考文献147件
  • Heo Kyung-Sun
    Aab Cardiovascular Research Institute, University of Rochester
  • Fujiwara Keigi
    Aab Cardiovascular Research Institute, University of Rochester
  • Abe Jun-ichi
    Aab Cardiovascular Research Institute, University of Rochester

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Emerging evidence is revealing the different roles of steady laminar flow (s-flow) and disturbed flow (d-flow) in the regulation of the vascular endothelium. s-flow is atheroprotective while d-flow creates an atheroprone environment. Most recently, we found unique atheroprone signals, which involve protein kinase C (PKC)ζ activation, elicited by d-flow. We and others have defined a novel role for PKCζ as a shared mediator for tumor necrosis factor alpha (TNF alpha) and d-flow, which cause pro-inflammatory and pro-apoptotic events in endothelial cells (ECs) in the atheroprone environment. Under such conditions, ONOO- formation is increased in a d-flow-mediated PKCζ-dependent manner. Here, we propose a new signaling pathway involving d-flow-induced EC inflammation via PKCζ-ERK5 interaction-mediated downregulation of KLF2/eNOS stability, which leads to PKCζ-mediated p53-SUMOylation and EC apoptosis. In addition, we highlight several mechanisms contributing to endothelial dysfunction, focusing on the relations bet-ween flow patterns and activation of reactive oxygen species generating enzymes. (Circ J 2011; 75: 2722-2730)<br>

収録刊行物

  • Circulation Journal

    Circulation Journal 75 (12), 2722-2730, 2011

    一般社団法人 日本循環器学会

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