Diabetic nephropathy (disease of the kidneys) is a complication of diabetes and affects nearly one-third of the diabetic population. Kidney failure results in people who suffer from diabetic nephropathy.
One of the main pathways that is activated in diabetic nephropathy is the JAK/STAT pathway. JAK and STAT are proteins that activate a series of proteins and thus creating cell conditions for the development of kidney disease. Inflammatory cells increase in the region of the kidneys due to the JAK/STAT pathway.
Researchers at the University of Madrid studied this pathway in diabetic mice with high blood sugar and high cholesterol. They introduced a molecule that mimics a protein in the JAK/STAT pathway. The protein’s name is SOCS1 or Suppressor of Cytokine Signaling-1.
The SOCS-1 mimic protein has the capability of blocking the JAK/STAT pathway and hence all the regulatory processes leading to diabetic nephropathy.
The stiudy was conducted in diabetic mice with high cholesterol. Hence, mice that were administered the SOCS-1 mimic reduced cell proliferation and reduced the expression of the target genes as well as the STAT protein.
Additionally, the SOCS-1 mimic also changed the expression of certain proteins in the process of diabetic nephropathy.
The researchers observed that this SOCS-1 mimic may be used for therapeutic purposes to halt the progression of diabetes to diabetic nephropathy. The results observed are in the early stages and need to be verified and confirmed further.
So far, there has been no therapy that has been successful in reducing the spread of diabetes to diabetic nephropathy. Use of this protein mimic may be just the right way to halt the progress of diabetes to diabetic nephropathy.
The researchers hope to develop a drug based on the protein mimic for clinical trials in the future in order to combat the condition of diabetic nephropathy.