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. 2013 Dec 19;2(6):e000376. doi: 10.1161/JAHA.113.000376

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© 2013 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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Figure 18. — Schematic representation of the molecular events activated by UnAG treatment following ischemia. Left: SC proliferation in response to muscle damage. Following muscle damage in response to microenvironmental stimuli, quiescent SCs undergo proliferation and differentiation to form new myofibers. Right: Proposed mechanism of UnAG action in response to ischemia. Following ischemic damage, quiescent SCs, protected from ROS generation by UnAG‐mediated SOD‐2 expression and miR‐221/222–driven p57^Kip2 posttranscriptional regulation, proliferate. As UnAG treatment leads to skeletal muscle regeneration, we hypothesize that the balance between p27^Kip1 and p57^Kip2 content or, alternatively, the expression of miRs different from miR‐221/222 or regulated by miR‐221/222 might be relevant for the entire regenerative process. FGF indicates fibroblast growth factor; HGF, hepatocyte growth factor; IGF‐1, insulin‐like growth factor‐1; miR, microRNA; ROS, reactive oxygen species; SC, satellite cell; SOD‐2, superoxide dismutase‐2; UnAG, unacylated ghrelin.