Protein, which is responsible for the equilibrium of calcium in cells, can delay the progression of chronic heart failure.

This is reported by MNT referring to employees of Okayama University.

This is a type 1 sodium-calcium transporter, or NCX1 protein.

It has long been known that it is involved in removing excess calcium from cells in the intercellular space. In this regard, NCX1 is extremely important for the heart - an intensively working muscle, where the level of calcium should always be subtly balanced.

With heart failure, increased activity of NCX1, but the researchers could not understand the role of this protein in the development of CHF. Now, Dr. Yuki Katanosaka and her colleagues have proven that overexpression of NCX1 contributes to myocardial remodeling. This protein causes changes in the size and shape of the heart muscle, necessary to adapt to the new, harsh conditions of its work.

To understand this, scientists derived genetically modified mice in which the expression of the NCX1 gene was controlled by a cardiospecific doxycycline-dependent promoter.

Without the administration of doxycycline, the activity of the NCX1 gene was practically zero, and in such animals, the chambers of the heart overstretched and thinned. The introduction of doxycycline (stimulation of the NCX1 gene) helped maintain the structure of the heart and adapt it to the needs of the organism.

"Moderate increases in the activity of the NCX1 gene can halt the development of heart failure by maintaining the required Ca2 + concentration within the cells," Cardiovascular Research.

medbe. en.

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