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These results suggest that ROS might increase mitochondrial biogenesis through a DNA damage/ATM/AMPK pathway.
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Also, DNP experiments suggest that the capacity of the OXPHOS machinery may not be intrinsically impaired in βIRKO cells; the improvement in oxygen consumption that we see in βIRKO and the rescued cells might be due to altered mitochondrial mass (Fig. S3B); that might increase total mitochondrial respiration.
This accumulation might inhibit HK activity and thereby increase mitochondrial ROS production (da-Silva et al. 2004).
We next investigated whether mitochondrial dysfunction might increase with ageing by assessing mitochondrial respiratory chain activity in muscle tissue of 2‐year‐old pink −/− zebrafish.
Accumulation of oxidative damage with age might derive from increased mitochondrial production of ROS unbalanced with the cellular response to oxidative stress (Balaban et al., 2005).
It is therefore difficult to speculate as to how reduced MRPL28 methylation might increase JIA risk, although mitochondrial dysfunction has been associated with autoimmune disease [ 29].
Based on our previous work, we hypothesized that SIRT3 might increase cell survival by regulating a mitochondrial protein that dictates cell viability.
Therefore, it is conceivable that mt-ND5 nt13708A variant might increase the susceptibility to MS by affecting the mitochondrial ROS production.
We also determined whether THC might increase ROS production in brain mitochondria and measured the mitochondrial free radical leak.
This might suggest that acetate oxidation increases mitochondrial respiration with concomitant increases in mitochondrial Ca2+.
It was therefore hypothesized that increasing mitochondrial function might be a valuable strategy to boost lipid oxidation, prevent lipid accumulation, and thereby treat insulin resistance.
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