Opening of Mitochondrial KATP Channels Triggers the Preconditioned State by Generating Free Radicals
By Tilley Pain, Xi-ming Yang, S. Critz, Yankun Yue, A. Nakano, Guang S. Liu, G. Heusch, M. Cohen, J. Downey. Circulation Research, 2000
725 citations recorded by the source corpus.
Subfields: Electrical and Electronic Engineering, Emergency Medicine, Pathology and Forensic Medicine
View Paper: https://www.semanticscholar.org/paper/c8fb67591d108c2d02e82bb879182f51b777e635
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In Electrical and Electronic Engineering
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Citations in the corpus
- Mitochondrial permeability transition pore opening during myocardial reperfusion--a target for cardioprotection. (2004, background): “This inhibition of respiration might be responsible for the increased mitochondrial production of ROS observed with diazoxide treatment [85–87], with the ROS then mediating IPC [68,88].”
- Mechanisms underlying acute protection from cardiac ischemia-reperfusion injury. (2008, background): “Diazoxide, an activator of the mitoKATP channel has been shown to increase ROS (71, 191), and addition of antioxidants has been shown to block the protection afforded by diazoxide as well as PC.”
- Preconditioning the myocardium: from cellular physiology to clinical cardiology. (2003, methodology): “(260) to propose a new paradigm incorporating mitoKATP channels and free radicals in PC’s signaling pathway leading to protection.”
- Glycogen synthase kinase-3β mediates convergence of protection signaling to inhibit the mitochondrial permeability transition pore (2004, neutral): “Figure 4A shows the cellular production of ROS induced by the prototypical PC-inducing agent, Dz, in agreement with previous observations (31).”