David M. Krzywanski

TL;DR: It is revealed that ozone increased vascular mtDNA damage in nonhuman primates in a fashion consistent with known atherosclerotic lesion susceptibility in humans, and inhaled ozone, in the absence of other environmental toxicants, promotes increased vascular dysfunction, oxidative stress, mitochondrial damage, and atherogenesis.

TL;DR: Results suggest that with respect to body composition parameters, mice housed singly are more similar to one another than are group-housed mice, most likely because of a reduction in environmental (predominately behavioral/social) effects.

TL;DR: The potential role for mitochondrial genetics and function in determining CVD susceptibility is considered from the standpoint that the original features that molded cellular function were based upon mitochondrial–nuclear relationships established millions of years ago and were likely refined during prehistoric environmental selection events that today, are largely absent.

TL;DR: It is demonstrated that NNT expression and activity are elevated in response to the mitochondrial dysfunction and oxidative stress associated with Ang II treatment, and is critical for the maintenance of mitochondrial redox balance and mitochondrial function.