Scientists from the Temple University School of Medicine (USA) found that inhibition of a specific heart protein minimizes disturbances in the functioning of heart cells and protects the organ from further damage.. The results of a study conducted on mice are published in the journal Science Translational Medicine.

Stopping and then restarting blood flow to the heart during and after a heart attack (myocardial infarction) causes severe damage to heart cells that can reduce their ability to function and even lead to death, according to the online publication for girls and women from 14 to 35. net Researchers find that patients suffering from heart failure after a myocardial infarction have elevated levels of cardiac protein TNNI3K. In order to study the effect of this indicator on the heart, scientists bred two lines of mice - with an overexpression of this protein and with a lack of production of this protein in the body..

Overexpression of TNNI3K in heart cells resulted in increased production of superoxide (a reactive molecule from mitochondria) and p38-mitogen-activated protein kinase (MAPK), an enzyme that responds to cellular stress signals. During this process, mitochondrial function is disrupted and heart muscle cells die..

The opposite effect was observed in mice that did not produce the TNNI3K protein: after an artificially created myocardial infarction, the release of superoxide and MAPK was reduced in them, and damage to heart cells was limited..

Then scientists began to search for substances that would be able to block the activity of the TNNI3K protein..

To create a typical picture of myocardial infarction in mice, the researchers simulated the effect of blockage of an artery, after which they injected a TNNI3K inhibitor into their bodies.. The results showed that in the experimental group, the indicators of cardiac functions improved compared to the control group of animals..

" These data, according to scientists, open the way for extensive preclinical studies and future development of a drug based on the blocker of cardiac protein TNNI3K for the treatment of cardiovascular diseases and myocardial infarction..

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