Autophagy against heart attack
To protect against heart failure after a heart attack, "eat" your heart!
Maria Perepechaeva, "First-hand Science"
As a result of a myocardial infarction, a section of the heart muscle dies, which can trigger the development of heart failure. What it will be depends on the process of scarring of the heart tissue and the degree of disruption of the structure and function of damaged and undamaged areas of the myocardium. A group of scientists from Italian universities and medical centers found that in this case, "the rescue of drowning people is the work of drowning people themselves," and in order to reduce the severity of the consequences of a heart attack, the processes of autophagy ("self–eating") need to be activated in the heart muscle.
Autophagy, one of the variants of programmed cell death, is an important link in the disposal of damaged or aging cellular organelles, "spoiled" protein molecules and unnecessary membranes. This orderly and well-regulated process of "garbage collection" is activated in cells in response to various negative stimuli, including cellular stress, infection and starvation. And also – with ischemic damage associated with insufficient blood supply to tissues, which we observe in ischemic infarction. However, the role of autophagy in the pathophysiology of cardiovascular diseases has not yet been fully established.
It is known that the autophagy process can be activated by the carbohydrate trehalose, which also protects cells from oxidative stress. This substance of natural origin, the molecule of which consists of two residues of glucose molecules, is considered harmless and is used as a sweetener and auxiliary component of medicines.
Italian researchers worked with laboratory mice in which a myocardial infarction was surgically simulated. During the first two days after the infarction, the animals were injected with trehalose intraperitoneally, and then for a month they drank water containing 2% of this carbohydrate. The control group received a saline solution or a sucrose solution.
It turned out that in mice receiving trehalose, mitochondria (the "power stations" of the cell) worked better, damaged cell organelles accumulated less, and the lysosomes themselves, capable of digesting damaged cell fragments, worked better. All this is evidence of the activation of autophagy processes. At the same time, these animals had higher heart performance, determined by electrocardiography and by studying the movement of blood through the vessels. These results indicate a weakening of the pathological processes of myocardial remodeling.
Scientists were able to confirm that trehalose improved the heart function of mice precisely by activating autophagy in experiments on mice heterozygous for the gene encoding the protein beclin – such animals are insensitive to autophagy activators. In these mice, trehalose did not really have a beneficial effect on heart function.
The molecular mechanisms of activation of autophagy by trehalose are still unknown, although scientists suggest that they are associated with the work of the signaling pathway of the enzyme kinase mTOR, the inhibition of which enhances the processes of disposal of damaged structures. But the main thing is that now there is evidence that such "self-eating" helps the heart muscle to cope with ischemic damage. According to scientists, this work may be the beginning of a new direction in the treatment of patients at high risk of heart failure after myocardial infarction.
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