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Breakthrough puts researchers on right path to creating drugs to fight heart disease

February 06, 17:35 UTC+3 MOSCOW
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MOSCOW, February 6. /TASS/. Researchers from Russia, the UK, and Switzerland demonstrated that the endothelin receptors type B have almost no influence of the fission of cells of unstriated muscles of vessels, the press service of Skolkovo Institute of Science and Technology said.

The results of the study imply that to cope with the vessel diseases, remedies need to be developed aimed at interacting with endotheline receptors type A (ETA) and time should not be spent on working with endotheline receptors B (ETB). The article describing the study has been published in the journal Hypertension.

"The experiments show no significant role of ETB receptors in the proliferation of smooth muscle cells. This is new information which may potentially save lots of money and effort just by pointing out the way which one should not follow, and namely, creating an ETB antagonist based anti-atherosclerotic drugs," commented Skoltech Professor Yury Kotelevtsev, Associate Director of Skoltech Center for Functional Genomics, and a coauthor of the study.

Endothelines are substances synthesized by the human body for constricting vessels. In order for them to function, they must be bound to corresponding receptors which are located in the vascular walls. These receptors can be classified into two types: A (ETA) and B (ETB). The ETA and ETB receptors govern the processes of vessels constriction and distension, as well as the growth of their tissues, and consequently play an important role in the evolution of some diseases, for instance, pulmonary hypertension and atherosclerosis.

To clarify the role of ETB receptor in the control of growth of smooth muscles cells, the scientists switched off the genes coding the receptor. Using a mouse, they damaged the arterial walls in the limb of the rodent to track the growth of vessel tissues without ETB receptors and found out that this receptor has almost no effect on the fission of cells after vessel damage.

According to Kotelevtsev, the scientists expected to come to sharply contradicting conclusions. But now, additional experiments have been scheduled, since these crucial results must be rechecked before finally being validated.

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