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Cellular cleansing saves from atherosclerosis

08.11.2016

Many diseases arise due to our own aged cells, which either can no longer perform their functions at all, or continue to do something, but incorrectly, not in the right way. The fact that a cell has grown old can be understood by the state of its DNA, in which more and more damage and errors accumulate over time - intracellular DNA repair systems simply do not have time to cope with them.

Usually, in this case, the cell immediately stops dividing - otherwise, with a whole "bouquet" of mutant genes "on hand", it has every chance of becoming malignant and giving rise to a cancerous tumor. But even having stopped dividing, the old cell continues to live in the body, synthesize some molecules, release them from itself into the external environment. Moreover, such molecules are capable of causing trouble to the surrounding normal cells and tissues.

Over time, the number of cells that are "neither alive nor dead" in the body only increases, but if you get rid of them, this literally helps to heal the body and increase life expectancy. You can get rid of them by turning on apoptosis, or a program of cellular self-destruction.

In the experiment of Darren Baker (Darren J. Baker) and his colleagues from the College of Medicine at the Mayo Clinic, genetically modified mice were used, in which the cell suicide program, apoptosis, could be triggered from the outside in aged cells. A special substance interacted precisely with such semi-working cells and turned the molecular "switch" that triggered cellular self-destruction.

Animals were kept on a fat-enriched diet for three months, then apoptosis was triggered in some, and the condition of the vessels was monitored. Signs of atherosclerosis in mice appeared quite soon, on the ninth day after they switched to fatty foods. But in those mice that were cleaned from old cells, atherosclerotic plaques appeared 60% less often - which is understandable, since deposits on the walls of blood vessels were rich in precisely aged cells. Among them, the most dangerous were immune macrophages, which consumed a lot of fat and turned on the inflammation that caused the plaque to grow.

In the later stages, the same "obese" macrophages secrete enzymes that make the plaque fragile, brittle, so that a piece can come off of it, swim somewhere with blood and eventually clog up some vessel. By the way, in the case when atherosclerotic plaques still formed in mice after the destruction of old cells, they were nevertheless stronger, and the likelihood that they would break, come off, and clog something somewhere remained small. .

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