ANY STRESS AT THE CELLULAR LEVEL MAY TRANSFORM CELLS INTO A DEFENSIVE MODE WHICH SLOWS DOWN CELLULAR SENESCENCE.THIS MEANS CELLULAR STRESSES EVEN LIKE DEFICIENCY OF ANTIOXIDANTS EXTENDED LIFESPAN WHICH WE HAVE TO UNDERSTAND FURTHER.
Mitochondria are recognized to play a key role in the aging process. In particular, the accumulation of mitochondrial reactive oxygen species (ROS) acts as the main driving force in the aging process. Although ROS was considered to be the main cause of oxidative damages in the past, recent studies have confirmed that appropriate low levels of ROS can be used as a signal molecule to initiate an adaptive response, which is beneficial to cells, particularly against the damage of cellular senescence. This process is called mitochondrial hormesis or mitohormesis. Upon activation, mitohormesis induces some cytoprotective mechanisms, which include activation of endogenous antioxidant system, upregulation of mitochondrial chaperons and unfolded protein response, changes in energy metabolism, and acceleration of the natural turnover rate of mitochondria. All these responses work synergistically to retard many aging processes and delay the onset and progression of age-related diseases. These findings are exciting because it suggests that mitophagy and mitohormesis may be a promising antiaging strategy, which solves the current clinical lack of treatment for aging-related disorders. Therefore, developing specific approaches to modulate mitohormesis may show therapeutic implications for many age-related processes such as cancer, diabetes, heart disease, and neurodegenerative diseases.
Source; https://www.sciencedirect.com/science/article/abs/pii/B978032390235900001X
