Aging results in the fact that the cells of our body renew themselves less and less well. The recycling process, called autophagy, is used by our cells to remove debris, such as poorly made proteins. Loss of this “quality control” mechanism is a hallmark of aging that leads to a buildup of toxic proteins leading to cell death. University researchers Case Western Reserve, in the United States, identified in the worm C.elegans, proteins controlling autophagy and prolonging their lifespan. Their results are published in the journal Kind Communication.
Control life expectancy
The scientists started from the observation that worms with excessive levels of a family of proteins, called KLF, lived longer and in better health than normal worms. They observed that the degree of these molecules decreased over time, and that worms without KLF could not maintain autophagy and therefore died earlier. Thus, by artificially increasing or decreasing the quantity of these proteins, they were able to make these worms live longer or shorter.
What is most exciting for scientists is that this group of proteins is also found in mammals. In mice, the decrease in KLF is linked to the particular aging of blood vessels, the main cause of many diseases such as hypertension. Furthermore, mice with excessive levels of KLF demonstrated a delay in vascular dysfunction associated with aging.
A path to new research
This study is a major step forward in understanding aging and age-related disorders. According to the researchers, the next step will be to study the precise mechanisms of autophagy in the cells that line blood vessels. Knowing what happens to our heart and our arteries is essential, because it is their proper functioning that determines our life expectancy. They will also seek strategies to target KLF proteins in humans and subsequently devise methods to slow down these processes.
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