How single gene may trigger heart attack

One single gene may activate mechanisms responsible for heart attack. An old cure may help.

Every second cells building our body divide creating new cells and this is a very complicated process. The major goal of that is to create cells which will maintain functions. The ones already used, you can say, lose their validity or mileage. During this process as it takes some time and comprises many steps, mistakes may happen. These mistakes are mutations of genes passed from one cell to another. And such a mutation may be or innocuous either hamper some functions of the new cell, sometimes all of them, sometimes may lead to a future disease when wrong copies of the basic gene begin to be duplicated in further cells division.

Heart attack is a very common incident throughout the world despite well-known wide range risks of this condition as well as more and more advanced interventions undertaken when it occurs along with measures against it. The most known risk factors include high blood pressure, obesity, high LDL cholesterol, diabetes and low physical activity. Particularly high cholesterol worries physicians as they see in it the main reason of atherosclerosis that can block blood vessels and this way contribute to lesions in the vessels as a consequence. And the true is that in many countries atherosclerosis due to high cholesterol is major reason of cardiovascular problems. But, as scientists from Spanish Centro Nacional de Investigaciones Cardiovasculares (CNIC) discovered there may be another cause of atherosclerosis. This cause is genetics which often makes us susceptible for problems with our health.

Dangerous gene for our heart


A single gene called TET2 wrong copy acquired during the division of blood stem cells may cause atherosclerosis. The blood vessels narrow slowing down the blood flow. This way it can lead to ischemia of heart and heart attack which is a sudden disruption of blood flow into the organ. The mechanism though is different than the one coming from an elevated level of cholesterol. The muted gene is stipulating a creation of subpopulation of blood cells which share the wrong copy of the gene and expand. The professional name of that is clonal hematopoiesis. The condition was linked to atherosclerosis but scientists were not clear whether it was a reason or consequence. It was also linked to the aging process and in fact it is one of biomarkers of aging. The condition is the most commonly shared by people after 50-ty in general population or sometimes before 20-ty in population of people with Down syndrome. Moreover, some sources link the somatic acquired mutation of the TET2 gene to cancer mutations among people in healthy population.

Scientists point out that the only way to prevent a heart attack due to clonal hematopoiesis that the same as cholesterol may harm walls of vessels is blocking the effect. The formation of lesions in the arterial wall underlines most cardiovascular disorders. The cure is colchicine, a substance gained from a certain plant and used from thousands of years in traditional medicine. Nowdays medicine uses medicines based on the substance to treat inflammatory conditions such as goat.

There is no major obstacle to its use for the prevention of cardiovascular disease in people with TET2 mutations.

says dr María Ángeles Zuriaga, who conducted the experimental studies at the CNIC and is the first author of the study published in the European Heart Journal. 

The medication is very cheap and available throughout the world. American FDA and European Medicine Agency granted their approval to the drug in prevention of cardiovascular disease in people with mutation in TET2 gene. The substance slows the development of atherosclerosis and thus alleviates the effects of clonal hematopoiesis associated with acquired mutations in the gene. The article was published in ,,Nature Medicine”


Comments

One response to “How single gene may trigger heart attack”

  1. Rafal, cardiologist Avatar
    Rafal, cardiologist

    The topic is interesting, the question is to what extent colchicine can prevent atherosclerosis in a wider patient population.

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