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- W1500066094 abstract "This chapter presents a new paradigm for the response to ischemia in the pulmonary circulation. The ischemic response depends on the sensing of decreased shear stress by the endothelial cell, resulting in the activation of membrane-associated NADPH oxidase, generation of O(in2)-, and activation of a signaling cascade. The initial response of the endothelium leading to NADPH oxidase activation is depolarization of the endothelial cell membrane, possibly a result of inactivation of membrane K(inATP) channels (KIR 6.2). ROS signaling leads to NO generation and cell proliferation. Thus, the K(inATP) channel may function as a “flow sensor” with the ability to initiate signaling subsequent to flow cessation. This response to altered shear stress may represent a physiological attempt to promote both vasodilation and the generation of new capillaries as mechanisms to restore blood perfusion.Key WordsEndothelial cellsmechanotransductionshear stresssuperoxide generationNADPHoxidaseKATP channeleNOS activationCa2+ influxcell proliferation" @default.
- W1500066094 created "2016-06-24" @default.
- W1500066094 creator A5022854559 @default.
- W1500066094 date "2005-01-01" @default.
- W1500066094 modified "2023-10-16" @default.
- W1500066094 title "Reactive Oxygen Species and Cell Signaling in Lung Ischemia" @default.
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- W1500066094 doi "https://doi.org/10.1007/978-1-59259-909-7_13" @default.
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