A new study, recently published by a British medical team, has revealed a new possible reason why wounds sometimes fail to heal. Researchers and doctors found that a molecule in the skin called MC1R — known as the gene responsible for red hair and fair skin — is constantly deactivated in chronic non-healing wounds. When this molecule in the skin was stimulated, inflammation levels decreased, and the wounds began to heal again. Although the gene is linked to pigmentation, its role is much broader; MC1R is found on various types of skin, immune, and vascular cells, meaning it controls several stages of the wound healing process. Healing is not just about closing a wound; it begins with necessary inflammation to remove damaged cells and microbes, after which this inflammation must gradually subside. In chronic wounds, the mechanism for switching off inflammation fails, leaving the skin stuck in an inflammatory phase for months. The researchers stated that they found three common features in chronic wounds: a dysfunction in MC1R, a dysfunction in its natural partner POMC, and continuous, unending inflammation. A topical drug restored skin healing. To improve the accuracy of the results, the researchers designed a new model of mice suffering from chronic wounds similar to human cases. When they applied a topical drug that activates MC1R, the results were clear: a sharp decrease in fluid secretion from the wound, recovery of the outer layer of skin and the beginning of closure, a reduction in inflammatory networks known as 'neutrophil traps' that impede healing. Even in small wounds in healthy animals, the drug improved blood flow and lymphatic drainage and reduced scarring, suggesting that the role of MC1R extends beyond disease states. The study suggests that targeting MC1R could be a new way to help the skin exit a state of chronic inflammation and begin to heal. The researchers hope that their findings will lead to the development of ointments or topical gels that patients can use themselves in the future.
