Pivotal role of NOX-2-containing NADPH oxidase in early ischemic preconditioning Robert M. Bell * , Alison C. Cave † , Sofian Johar † , David J. Hearse * , Ajay M. Shah † and Michael J. Shattock * ,1 * King’s College London, Cardiac Physiology, Cardiovascular Division, The Rayne Institute, St. Thomas’ Hospital, London. SE1 7EH, UK; and † King’s College London, Department of Cardiology, Cardiovascular Division, Guy’s, King’s and St. Thomas’ School of Medicine, Bessemer Road, London. SE5 9PJ, UK 1 Correspondence. King’s College London, Cardiac Physiology, The Rayne Institute, 4th Floor, Lambeth Wing, St. Thomas’ Hospital, London. SE1 7EH, UK. E-mail: Robert.m.bell@kcl.ac.uk <h3>SPECIFIC AIMS</h3> Preconditioning is a powerful, inducible endogenous adaptive mechanism that protects the heart against injurious ischemia/reperfusion injury. A role for reactive oxygen species (ROS) has been identified in the myocardial preconditioning signal transduction pathway, though the source of these ROS remains elusive. Cardiac myocytes have recently been demonstrated to contain a phagocyte-type NADPH oxidase, a potent source of ROS. Pharmacological preconditioning triggers, such as angiotensin II, are known to up-regulate NADPH oxidase activity and ROS synthesis in the context of cardiac hypertrophy, a response abrogated by the targeted deletion of the NADPH oxidase
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Pivotal role of NOX-2-containing NADPH oxidase in early ischemic preconditioning
Bell, Robert M.; Cave, Alison C.; Johar, Sofian; Hearse, David J.; Shah, Ajay M.; Shattock, Michael J.
Follow The FASEB Journal
, Volume 19 (14): 2037
Fed of American Socs for Experimental Biology – Dec 1, 2005
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