One of the most disappointing and debilitating complications of diabetes is the development of wounds on the foot or lower leg. Once they form, they can continue for a considerable length of time, prompting to painful and dangerous infections. New research reveals the role of a specific protein in keeping up these wounds and suggests that turning around its belongings could enable guide to wound healing in patients with diabetes.
Researchers found that a particular protein, thrombospondin-2 (TSP2), is raised in wounds of patients with diabetes and in addition in animal models of diabetes. To decide whether TSP2 contributes to delay wound healing, analysts genetically expelled thrombospondin-2 from a mouse model of diabetes and observed improved enhanced healing. The study shows that TSP2 could be a target for a specific therapy for diabetic wounds.
Treatment for these wounds is mostly limited to standard wound care, such as moist bandages, removal of damaged tissue and footwear that reduces pressure on the wound. Despite these measures, the wounds often persist. In the most severe cases, it becomes necessary to amputate the affected foot or lower leg.
Most previous work on wound healing in diabetes has concentrated on the types of cells that are associated with wound healing such as skin cells, immune cells and the cells that form blood vessels. By contrast, research focuses on TSP2, a segment of the extracellular matrix. The extracellular matrix is a meshwork that serves as the structural foundation for cells, similar to the scaffolding used in construction. Thrombospondin-2 is a segment of the extracellular matrix that impacts how the matrix is framed, and also the development and communication of different types of cells that develop within the matrix.
They also analysed the factors that influence how much TSP2 the body produces. That part of the study revealed that TSP2 production increases when blood sugar levels are higher, explaining why people with diabetes have higher levels of TSP2 than people without diabetes.
Currently, lab is developing engineered biomaterials derived from extracellular matrix that lacks TSP2. Researcher’s idea is to apply such materials to diabetic wounds in mouse models in order to evaluate their efficacy. Going forward, additional research will focus around either inhibiting the function or preventing the production of thrombospondin-2 in diabetic wounds.
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