Anna Hartz
Millions of people around the world live with wounds that simply will not heal.
These wounds are often caused by diabetes, poor blood flow, or prolonged pressure. They can be painful and carry a high risk of infection. Chronic wounds can seriously reduce quality of life. In severe cases, they can even lead to amputation.
Wounds That Never Heal
Current treatments, like dressings, antibiotics, and repeated doctor visits, often manage symptoms but do not address the root cause. For many, the problem never fully goes away. Recent research from a team at University of Edinburgh gives a new perspective on why some wounds remain open. It also points to a possible new way to treat them.
They found that a molecule in the skin called MC1R is consistently disrupted in chronic wounds, writes Videnskab. Activating this molecule allows the skin to reduce inflammation and start healing. Most people know MC1R for a completely different reason: it controls red hair and very fair skin. But the gene does much more than affect pigment.
MC1R is present in many types of skin cells, including immune cells, keratinocytes, fibroblasts, and the cells lining blood vessels. This means it can influence multiple key steps in the healing process. Healing is more than just closing a wound. The skin first triggers an inflammatory response. This is the body’s defense against infection or injury. Once the inflammation is properly “switched off,” the body can repair itself.
Tested on Mice
If that switch fails, wounds stay inflamed for months. They studied human tissue samples from diabetic foot ulcers, venous leg ulcers, and pressure sores. All showed the same problem: the mechanism that normally reduces inflammation was disrupted. MC1R and its partner molecule, POMC, were out of balance.
They tested this in mice with a non-functioning MC1R gene. Their wounds healed slowly and had persistent inflammation, similar to human chronic wounds. Applying a drug that activates MC1R significantly improved healing. Inflammation decreased, blood vessel growth increased, and the skin began to close over the wound.
The treatment also reduced harmful immune activity and scar formation. Even in normal wounds, activating MC1R improved blood flow and lymphatic drainage.
This research shows that MC1R plays a central role in coordinating skin repair. When the pathway is disrupted, inflammation continues. When MC1R is activated, inflammation subsides and healing resumes. Targeting MC1R could lead to new treatments for millions of people living with chronic wounds.
Sources: Videnskab
