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. 2016 Mar 3;118(5):856–866. doi: 10.1161/CIRCRESAHA.115.307918

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© 2015 The Authors.

Circulation Research is published on behalf of the American Heart Association, Inc., by Wolters Kluwer. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDervis License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

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Figure 3. — Mitochondrial hydrogen peroxide (H₂O₂)–mediated flow-mediated dilation (FMD) after inhibition of telomerase. H₂O₂ levels were analyzed using the H₂O₂-specific florescent probe PYI (peroxy yellow 1) targeted to mitochondria (MitoPYI) in vessels from non–coronary artery disease (CAD) subjects. A, Representative image; numbers represent florescent intensity above background. B, Summary of florescence intensity at 5 minutes after initiation of flow. Specificity of the probe for H₂O₂ was confirmed using polyethylene glycol-catalase (Peg-Catalase). C, An inhibitor of electron transport chain complex I (rotenone) or a mitochondrial-targeted reactive oxygen species (ROS) scavenger (MitoTempol) inhibited FMD after telomerase inhibition. N=4. *P<0.05 2-way analysis of variance (ANOVA) RM (dose response curve) or t test (fluorescence data) with Tukey post hoc.