Thus, the G protein-coupled mtCB1 receptors regulate memory processes via modulation of mitochondrial energy metabolism.
Although the pathological impact of chronic mitochondrial dysfunctions in the brain is well established1,2, the involvement of acute modulation of mitochondrial activity in high brain functions, including learning and memory, is unknown.
Recently, NO-donors have been proposed as promising therapeutic options for breast, liver and skin cancers50 and, in this perspective, we reasoned that the anti-metastatic role of AA6 might be not only associated to its modulation of mitochondrial metabolism and TET activation but also to an effect on endogenous NO synthesis.
Taken together, these data suggest that protective effects of quercetin against oxidative injuries of H9c2 cardiomyoblasts may be achieved via modulation of mitochondrial dysfunction and inhibition of caspase activity.
Although integrin-mediated signaling in cancers has been shown to promote their resistance to IR treatment15,16,17,18 as well as the enhancement of their invasiveness after IR19,20,21, involvement of the regulation of intracellular ROS levels in these contexts, possibly through the modulation of mitochondrial functions and/or positioning, has remained unknown.
Previous discovery of a mitochondrial progesterone receptor, PR-M, has opened up the possibility of direct, ligand-dependent modulation of mitochondrial activity.
Furthermore, modulation of mitochondrial oxidative stress could play a beneficial role in the prevention of this devastating complication of sepsis.
Mitochondrial impairment (including modulation of mitochondrial dynamics-associated protein content), enhanced oxidative stress, and an inflammatory response were also detected in our experimental paradigm.
Therefore, it is possible that modulation of mitochondrial dynamics may be a useful therapeutic modality for preventing neurodegenerative disorders because microglia-mediated neuroinflammation is associated with neurodegenerative processes.
Interestingly, a series of studies conducted in yeast showed that inhibition of TOR signaling extended life span via modulation of mitochondrial respiration, function, and gene expression.
An important strategy in this regard is the modulation of mitochondrial ROS generation, which is downregulated in cancer cells by shifting to aerobic glycolysis.
