According to information of the Robert Koch-Institute more than 4.5 million Germans are suffering from a Form of Diabetes. Due to the significant result of faster progress is the disease in the research value of Gold. Austrian scientists have now made a first breakthrough that can change the management of the disease in the future.
In Germany alone, more than 4.5 million people are suffering from Diabetes type I or II. Experts fear that this number will rise significantly in the future. Anyone who suffers from Diabetes, has diseases there is an increased risk for a result such as kidney failure, blindness, heart attacks or strokes.
Scientists, of blood cells from stem cells to form
To prevent this, it is important to understand the disease process better. To this aim, researchers at the Institute of Molecular biotechnology of the Austrian Academy of Sciences, in short, IMBA now, come a little closer: you have done it, real human blood vessels from stem cells to replicate. This means that you are no longer dependent on animal experiments, the results of which often can only be bad to people. Instead, you can explore the disease now in human tissue.
The team of researchers led by Reiner Wimmer has been able to gain first insights. They tried various chemical Compounds in the diabetic blood vessels, in order to prevent the expression of the disease. They found that none of the currently approved Diabetes medications had an effect on the course of the disease.
The new model system will also help in cancer and Alzheimer’s research
They discovered, however, that certain proteins are significantly involved in the thickening of the basal membrane, which is typical in diabetic patients. This restricts the oxygen supply to the cells. It managed to block the protein with a molecule, it would be a new approach for the treatment of Diabetes. The researchers hope their model system, but also a new impetus to cancer and Alzheimer’s patients, because the blood vessels in the progression of this disease progression will play a big role.
