Read on the topic aging research and one will soon enough arrive at a consideration of mitochondria, their function and dysfunction. They are everywhere in the literature. These organelles are responsible for processing nutrients into chemical energy stores, and also play a role in a variety of important mechanisms in cell growth and cell death. They mediate many beneficial cellular responses to stress via generation of reactive oxygen species in greater or less amounts. Further, they are a primary target for the cellular maintenance processes of autophagy, as when mitochondria malfunction they can cause serious harm to a cell and its surroundings. That portfolio of functions and concerns is connected to all of the present methods of metabolic alteration shown to modestly slow aging in laboratory animals.
Most of these methods utilize the induction of stress response mechanisms, particular those involved in calorie restriction, the reduction of nutrient intake, which overlap with responses to exercise, to heat, to toxins, and to lack of oxygen. Altered mitochondrial function appears frequently as a central mediating mechanism. Calorie restriction itself appears to depend on increased levels of autophagy – and as soon as autophagy is involved one has
Article originally posted at