Huntington's disease (HD) is caused by a dominant polyglutamine expansion within the N-terminus of huntingtin protein and results in oxidative stress, energetic insufficiency and striatal degeneration.
These are released from mitochondria to the cytosol in response to apoptotic signals, like DNA damage, oxidative stress, energetic catastrophe, viral infection, endoplasmic reticulum (ER) stress or xenobiotic intoxication.
p53 tumor suppressor is activated in cells in response to a variety of stimuli, including DNA damage, hypoxia, oxidative stress, and the energetic stress [12], [13].
Inefficiencies in brood production place energetic stresses on honey bee colonies.
During energetic stresses, the activation of AMPK limits protein synthesis and cell growth to protect against apoptosis through the TSC2/mTOR pathway.
Indeed in cells lacking a functional LKB1 pathway, metabolic stress has been demonstrated to result in rapid apoptosis as the cells are unable to sense energetic stresses and activate mechanisms to restore energy homeostasis [ 44].
In this context, it has been demonstrated that cytokine levels, oxidative stress, and energetic metabolism alterations seen early after sepsis may persist for up to 30 days and this could be associated with cognitive damage [24 26].
Additional proteins such us pi and omega classes glutathione transferases, ATP synthase D chain, were also found to be up-regulated, suggesting that the enzyme belonging to the cellular detoxification system against oxidative stress and energetic metabolism may have a key role in the cellular response to radiation injury.
Both the high intrinsic film stresses due to high energetic film growth and the huge difference in elastic properties of films and polymer substrates result in hierarchical and self-adapting nanowrinkling phenomena.
The onset of cellular senescence is thought to protect against the initiation of tumor formation in response to certain cellular stresses, including genotoxic and energetic stresses [ 48].
