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The "perfect" anti-inflammatory has been found
Last reviewed: 01.07.2025
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Scientists have discovered a previously unknown function of the TRPC6 protein, which could become a new component for more effective action of anti-inflammatory drugs.
Scientists from the Department of Clinical Research at Cincinnati Children's Medical Center have discovered that a protein called TRPC6 may be a key part of the body's recovery from various injuries caused by diseases.
For example, after a heart attack, TRPC6 helps tissues repair and heal. Researchers have found that it causes fibroblasts to transform into myofibroblasts, which in turn secrete substances called extracellular matrix, which are important components for wound contraction and scarring.
"Our findings suggest that TRPC inhibitors may be an excellent anti-fibrotic or anti-inflammatory treatment for heart failure, muscular dystrophy, and pulmonary ventilation disorders in which fibrosis is a major problem," said Jeffrey Molkentin, lead author of the study and a natural scientist at Cincinnati Children's Hospital Medical Center. "This needs to be further studied to see how clinically applicable our findings are."
Our body needs a certain amount of the substance, not too low, but not excessive, which is capable of healing a wound. Otherwise, its excess can cause compaction of connective tissues (fibrosis), which will lead to serious complications.
To determine the safe dose of the protein, experts will need additional clinical trials to find the ideal balance that will make it possible to use this substance for therapeutic purposes.
Before this study, TRPC6 had not been linked to fibrosis, although scientists knew it was involved in cellular functions in the kidneys, skin cells, and hippocampal neurons in the brain.
The specialists conducted their research on rodents. As a result of the action of the TRPC6 protein, the injured tissues of the animals were restored faster. The scientists affected TRPC6 on the cells of embryonic fibroblasts of mice, cardiac fibroblasts of rats and fibroblasts of human skin. Under the influence of the protein, fibroblasts were transformed into myofibroblasts, while fibroblasts not infected with TRPC6 remained in their previous state. In mice whose bodies did not have enough TRPC6, the healing processes after injuries were slow and complicated.