Why the study?
Does Nox2 induce mitochondrial superoxide production via reverse electron transfer in Angiotensin II-mediated hypertension?
Does Nox2 induce mitochondrial superoxide production via reverse electron transfer in Angiotensin II-mediated hypertension?
Nox2-induced mitochondrial ROS via reverse electron transfer is identified as a potential new mechanistic target for the pharmacological treatment of hypertension.
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May nominate mitochondrial superoxide as a hypertension target; hypothesis-generating in animals, clinical translation remains untested.
These studies show that Nox2 stimulates mitochondrial ROS by activating reverse electron transfer and both mitochondrial O2(•-) and reverse electron transfer may represent new pharmacological targets for the treatment of hypertension.
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Dikalov et al. (2013) studied this question.
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