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. 2012 Nov 27;124(Pt 6):403–411. doi: 10.1042/CS20120239

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© 2013 The author(s) has paid for this article to be freely available under the terms of the Creative Commons Attribution Licence (CC-BY)(http://creativecommons.org/licenses/by/3.0/) which permits unrestricted use, distribution and reproduction in any medium, provided the original work is properly cited.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original work is properly cited.

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The results suggest a potentially mtROS-mediated increase in AMPK activity in patients with CAD and T2D. The mtROS in question are likely to be downstream derivates of H₂O₂, such as lipid peroxidation products. AMPK may therefore be part of a feedback or adaptive mechanism with a role in defence against oxidative stress in the endothelium, attenuating pro-inflammatory signalling and regulating expression of antioxidant genes, including SOD2. However, increased kinase activity does not appear to be sufficient to stimulate activation of eNOS, in patients with T2D.