Discovering the mechanism involved in the contraction of heart muscle

German scientists at Bochum University discovered a mechanism to control the elasticity of Titin protein, deciding on the hardening of the heart muscle.

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The findings were published in the medical journal Cells and Journal of Cell Biology on March 19. In it, explain why after being pressured like pain, the heart often loses its ability to contract.

According to the study, T itin - the largest protein in the human body - acts like a muscle cell stretcher or stretcher.

Artwork: scitechdaily.com

In this kiln area there are a number of protein units - also known as immune globulin regions - that are sequenced as pearl chains.

Under conditions of pressure such as acute cardiomyopathy, the ovary area is excessively stretched and the area of ​​immune globulins is exposed.

Because the globulin region cannot return to the original structure, it reduces the elasticity of the heart wall and the protein Titin cannot perform the sensing function against the mechanical stresses of heart disease. This limits the function of the heart's contractile function.

The study also showed that the proteins in the exposed area of ​​Titin protein would move and prevent the "pearls" of the ovens from connecting. This prevents pathological changes related to the elasticity of Titin when there are chronic heart attacks or heart disease.

Besides, scientists also discovered that cardiac muscle cells also have mechanisms to protect the elastic area of ​​Titin protein against the effects of pressure.