Chronic wounds, especially diabetic foot ulcers, are a serious problem for people with diabetes.
These wounds heal slowly and often never fully recover, mainly because the body struggles to grow new blood vessels in the damaged area.
Without this blood vessel growth, or angiogenesis, the tissue can’t get the oxygen and nutrients it needs to repair itself.
This slow healing process can lead to infections, hospital stays, and even amputations. Current treatments often fail to address one of the main causes of poor healing in diabetic wounds — a protein called thrombospondin-1 (TSP-1), which blocks the growth of new blood vessels.
Now, researchers in China have developed a new wound dressing that may change how these wounds are treated. In a study published in the journal Burns & Trauma, the team combined two advanced technologies: small extracellular vesicles (sEVs) loaded with a microRNA called miR-221-3p, and a GelMA hydrogel.
The microRNA works by targeting and reducing TSP-1 levels, removing a major barrier to blood vessel growth. The GelMA hydrogel acts as a carrier, slowly releasing the treatment at the wound site while also mimicking the body’s natural tissue structure.
The research showed that high blood sugar in diabetic wounds increases TSP-1 levels in endothelial cells, which line the inside of blood vessels. This stops the cells from multiplying and moving to form new vessels.
By delivering miR-221-3p directly to the wound, the scientists were able to lower TSP-1 and restore the cells’ ability to grow and migrate. The engineered vesicles carrying miR-221-3p were placed inside the GelMA hydrogel, creating a system that released the therapy over time right where it was needed.
In tests with diabetic mice, the results were striking. The treated wounds healed much faster and formed more new blood vessels than those in control groups.
After just 12 days, the wounds treated with the new hydrogel had closed by about 90%, compared to much slower healing in untreated wounds. The improvement in blood vessel growth was also clear, with better oxygen and nutrient supply to the healing tissue.
Dr. Chuan’an Shen, one of the lead researchers, said that the work shows how combining molecular biology with tissue engineering can bring major advances in medicine.
Targeting TSP-1 with miR-221-3p inside the hydrogel not only fixed problems in endothelial cells but also kept the treatment working locally over time. He believes this method could greatly improve quality of life for people with chronic wounds.
This new technology could also be used beyond diabetic ulcers. The same approach might help heal other chronic wounds caused by poor blood flow, or even be adapted for regenerating bone, cartilage, and other tissues.
While the results in animals are promising, more research and human trials are needed before the treatment can be widely used. If future studies are successful, combining miRNA-based therapies with biocompatible hydrogels could become a key part of regenerative medicine, giving patients faster and more complete healing.
This study addresses a major gap in diabetic wound care by tackling the root cause of poor healing — the suppression of new blood vessel growth. By using miR-221-3p to reduce TSP-1 levels and delivering it through a GelMA hydrogel, the researchers achieved faster healing and better tissue repair in animal models.
The approach stands out because it combines targeted molecular therapy with a delivery system that works over time at the site of injury. If proven effective in humans, this method could become a groundbreaking treatment for not only diabetic foot ulcers but also a wide range of chronic wounds.
If you care about diabetes, please read studies about The hidden connection between cancer and diabetes uncovered and findings of Scientists find the best way to help people with diabetes lose weight.
For more information about diabetes, please read studies about Widely prescribed drug may increase sudden cardiac arrest risk in people with diabetes and findings of These common drugs linked to sudden cardiac arrest in people with type 2 diabetes.
The study is published in Burns.
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