Found an "ideal" anti-inflammatory drug
Last reviewed: 16.10.2021
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Scientists have discovered a previously unknown function of protein TRPC6, which can become a new component for the more effective action of anti - inflammatory drugs.
Scientists from the Department of Clinical Studies at the Cincinnati Children's Medical Center have found that a protein called TRPC6 can be a key link in the process of restoring the body after various injuries caused by diseases.
For example, after a heart attack, TRPC6 helps tissues recover and heal. As the researchers established, under its influence, fibroblasts are transformed into myofibroblasts, which in turn release substances called extracellular matrix, important components necessary for contraction and scarring of wounds.
"Our research suggests that TRPC inhibitors can be an excellent antifibrotic or anti-inflammatory agent in the treatment of heart failure, muscular dystrophy and pulmonary ventilation disorders in which tissue fibrosis becomes a big problem," said Jeffrey Molkentin, lead author and natural scientist at the medical the center of the children's hospital in Cincinnati. "This issue should be studied in more detail, in order to find out how much our discovery is clinically applicable, that is, in practice."
Our body needs a certain, not too low, but not excessive, amount of substance that can heal the wound. Otherwise, from its excess, condensation of connective tissue (fibrosis) may occur, which will lead to serious complications.
To find out a safe dose of protein, experts will need additional clinical trials, with which an ideal balance will be found, which will make it possible to use this substance for therapeutic purposes.
Prior to the current study, TRPC6 was not associated with fibrosis, although scientists were aware of its involvement in the cellular functions of the kidneys, skin cells and hippocampal neurons of the brain.
The specialists conducted their studies on rodents. As a result of the action of TRPC6 protein, the injured tissues of animals recovered more quickly. Scientists exposed TRPC6 to cells of embryonic fibroblasts of mice, rat cardiac fibroblasts and human skin fibroblasts. Under the influence of protein, fibroblasts were transformed into myofibroblasts, whereas fibroblasts not infected with TRPC6 remained in their original state. In mice in which there was not enough TRPC6, the processes of wound healing after injuries were slow and with complications.