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. 2013 Aug 26;1(1):411–417. doi: 10.1016/j.redox.2013.08.004

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© 2013 The Authors

This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-No Derivative Works License, which permits non-commercial use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Fig. 5 — Working model for the mechanism of Ang II-induced SIPS in hVSMC. Ang II acts via the AT1 receptor to illicit superoxide production via a NADPH-linked process. Cytoplasmic oxidants, mitochondrial superoxide/mitochondrial function are necessary for the development of SIPS. This mechanism invokes NADPH oxidase-mitochondrial cross-talk via oxidant generation; the working hypothesis is that firstly NADPH oxidase is activated by Ang II which leads to stimulation of mitochondrial superoxide resulting in a feed-forward amplification of NOX activity and subsequent downstream induction of SIPS.