Useful stress

Mitochondrial stress helped slow down aging

Anna Kaznadzei, N+1

Mild stress, which reduces the efficiency of mitochondria, can stop the programmed aging processes of the body. This is due to the cessation of inhibition of the synthesis of heat shock proteins that regulate the stability of protein molecules in cells, biologists from the USA and the UK report in an article published in Cell Reports (Labbadia et al., Mitochondrial Stress Restores the Heat Shock Response and Prevents Proteostasis Collapse during Aging).

A group led by Richard Morimoto from Northwestern University experimented with the roundworm Caenorhabditis elegans, a model organism whose cells work much like processes in the human body. Almost immediately after the worms become adults, metastable proteins in their cells begin to form clots, as the mechanisms that maintain their shape and prevent sticking stop working. This is one of the programmed aging processes. If earlier it was believed that the aging of the body occurs solely due to the accumulation of unavoidable cell defects over time, then in recent years it has become clear that many of the aging processes occur in a programmed way, including through the regulation of cellular expression.

One of the important factors regulating the expression of genes responsible for the mechanisms of maintaining proteostasis (stability of protein molecules) is the heat shock protein HSF-1. Between the first and second day of life at the adult stage of C.elegans, the level of this protein is significantly reduced. The scientists conducted a comparative analysis of the work of C.elegans genes, turning them off one by one using RNA interference and checking how well the worms would respond to heat shock. It turned out that the inhibition of HSF-1 is associated with the work of 11 genes – their shutdown restored the response to heat shock by at least 50 percent. One of the genes performing the same functions as the gene of the human cytochrome c oxidase of the electron transport chain (ETC) of mitochondria restored this response completely.

Further experiments have shown that various methods of not too significant disruption of the mitochondria can enhance the response to heat shock and increase the overall stability of cells. Among the ways to "irritate" mitochondria, scientists call the effects of chemicals such as rotenone and antimycin, as well as the influence of certain types of bacteria. Among other things, such stress supported proteostasis, preventing the accumulation of protein clots in cells. This, in turn, led to the prolongation of the worms' life. Previously, it was known that disruption of the work of the ETC can prolong the life of the organism, but it also caused deterioration of health, a decrease in the ability to reproduce and a reduction in the number of offspring. However, researchers have now found that a low level of stress acting through mitochondria on the expression of heat shock genes prolonged the life of C.elegans without causing similar side effects.

In general, scientists describe a complex system of interaction between proteostasis, the work of mitochondria and heat shock proteins, the impact of which can lead to a decrease in the rate of programmed aging processes. In the future, they intend to continue studying it. And you can read about the targeted removal of aging (senescent) cells from the body here.

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