Speeding up diabetic wound healing
Releasing the 'healing brake' on our immune system
July 7, 2022
Chronic skin wounds affect many diabetic patients, with a negative impact on their quality of life. Sophia Maschalidi (VIB-UGent) discovered how to accelerate wound healing and decrease the risk of infection.
Key facts (estimates for 2021 from the International Diabetes Federation)
- Globally, an estimated 537 million adults have diabetes.
- Around 75% of them live in low- and middle-income countries, and roughly half are undiagnosed.
- Diabetes care represents almost 10% of global health expenditure.
- Diabetes is responsible for almost 7 million deaths every year.
Release the brake
The skin is the largest organ of the human body. It helps us sense the environment through touch, heat and cold, and acts as a protective barrier against dehydration and pathogens. When injured, cells of our immune system remove the dead cells and restore the skin. Delay of this healing increases the risk of wound infection and severe inflammation. This is a concern, especially for diabetics. Almost 1 in 10 people worldwide suffer from diabetes-related complications, including slower wound healing.
“High blood sugar levels often slow wound healing, leading to discomfort and health risks for the patient. In our study, we found a ‘healing brake’ that is active during recovery. Releasing that brake resulted in faster wound healing in diabetic mice,” says Sophia Maschalidi (VIB-UGent Center for Inflammation Research).
Cleaning helps the healing
In healthy skin, old cells undergo cell death and are replaced by new cells. This removal of dying cells – efferocytosis – happens with the help of many different cells in our body, but a large part is done by phagocytes that are components of our immune system.
“Defects in efferocytosis go hand in hand with chronic inflammation. Gaining insight into the regulation of this process could reveal unexplored ways to prevent or treat skin inflammation and improve wound healing,” says Esther Hoste (VIB-UGent Center for Inflammation Research), who collaborated on this project.
One type of phagocyte involved in efferocytosis is the dendritic cells (DCs). DCs can be found in almost every tissue and clean up dead cells by eating them. While studying the genetic profile of DCs engulfing cells, the team of Kodi Ravichandran (VIB-UGent Center for Inflammation Research) found one particular protein – SLC7A11 – negatively regulating DC-mediated efferocytosis.
“SLC7A11 slows down efferocytosis by dendritic cells. When we treat dendritic cells with a drug that inhibits SLC7A11 function, we improve dead cell clearance by the DCs,” Sophia explains.
As the removal of cell debris from wounds is crucial to avoid infection and promote tissue repair, deciphering the regulatory mechanism(s) behind healing is a key step toward better wound care.
Prof. Kodi Ravichandran: “We were thrilled that inhibiting SLC7A11 in diabetic mouse models accelerates wound healing. This has potential for novel strategies to treat slowly healing wounds in diabetes patients or other chronic inflammatory conditions of the skin.”
Maschalidi et. al., Nature, 2022
Questions from patients
A breakthrough in research is not the same as a breakthrough in medicine. The realizations of VIB researchers can form the basis of new therapies, but the development path still takes years. This can raise a lot of questions. That is why we ask you to please refer questions in your report or article to the email address that VIB makes available for this purpose: [email protected]. Everyone can submit questions concerning this and other medically-oriented research directly to VIB via this address.