Cardiovascular diseases: New therapy for better vascular function

Researchers find the connection between the increased number of receptor proteins in the blood and the development of cardiovascular diseases.

A specific protein in blood vessel cells is largely responsible for the development of cardiovascular and vascular diseases: If the “thromboxane A2 receptor” is present in too large quantities, this impedes the formation of new blood vessels. This is what a research team led by Prof. Ralf Benndorf from the Martin Luther University Halle-Wittenberg (MLU) discovered. In the journal Arteriosclerosis, Thrombosis, and Vascular Biology he describes the underlying process for the first time. The findings could help to develop new treatment options for cardiovascular diseases.

Endothelial cells: The regulators in the blood

The formation of blood vessels is a complex process. “Like the cogs in a clockwork, various inhibiting and stimulating processes have to mesh with one another. Blood vessel endothelial cells play a crucial role in this. They regulate the exchange between blood and tissue,” says Benndorf.

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The researchers examined a protein that is important for hemostasis: the thromboxane A2 receptor causes blood platelets to stick together and is involved in the narrowing of blood vessels. “It was already known from patients with cardiovascular diseases and pathological changes in the blood vessels that there is an increased number of these receptor proteins in their blood vessels,” Benndorf continues. However, it was previously unclear whether this finding has any clinical relevance, i.e. whether there is a connection between the increased number and the development of the diseases.

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This is exactly what the researchers were able to show in their new study, decoding an extremely complex interaction that is triggered by this receptor protein.

On the trail of the secret

The problem arises when there is too much of the protein in the blood vessels: “The receptor ensures that the pro-inflammatory enzyme cyclooxygenase-2 is produced in excess. This in turn produces messenger substances that activate the receptor,” explains Benndorf. This constant and self-reinforcing activation of the receptor in the blood vessel cells means that the cells are hardly able to form new blood vessels. The function of the blood vessel endothelial cells is also significantly restricted. “Under the microscope you can see how the cells are under increased voltage when the receptor density is increased,” says Benndorf.

It is not yet possible to say with certainty why the protein is found in increased amounts in the blood vessel cells of people with cardiovascular diseases. “However, it is a promising biomarker and an interesting target for pharmacological interventions,” said Benndorf. With the help of substances that block the effect of the receptor and the enzyme, the harmful effects in the cells could be reversed. “In patients in whom the thromboxane A2 receptor is present in large quantities in blood vessels, targeted inhibition of the receptor could therefore represent a new therapeutic option to improve vascular function and regeneration.”

Studies give hope for therapeutic benefits

The first drugs targeting the protein are already in clinical trials for other applications. “Although the substances have not yet been approved, the results of the clinical studies indicate that they are well tolerated and can improve vascular function,” says Benndorf. The current investigations took place in cell cultures and laboratory animal studies. Before an application in humans is possible, further work on a possible therapeutic benefit in preclinical disease models must be carried out.

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This article is based on a press release from Martin Luther University Halle-Wittenberg. We have linked the original publication here and in the text.

Image source: Heather Barnes, unsplash



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