Grant: CIHR Fellowship

People living with diabetes are much more likely to develop kidney disease than people who do not have diabetes. Often, when kidney disease happens it develops slowly over years. This is called chronic kidney disease, or CKD. These days there are several treatments available that can help slow the worsening of CKD. At other times, kidney damage can happen very quickly, for example if someone gets sick for another reason or if they have major surgery. This is called acute kidney injury, or AKI. People with diabetes are also much more likely to develop AKI than people who do not have diabetes; and, if a person has AKI, they are at increased risk of developing CKD in the future. However, unlike CKD, there are no specific treatments for AKI in diabetes beyond what is known as supportive care. In my project, I am exploring a new treatment opportunity for AKI in diabetes. This opportunity is built around a protein present in cells called STING. STING works like a master controller. When it is turned on, it tells cells to make proteins that can worsen kidney damage through a process called inflammation. It also controls how cells behave and, in particular, how our body's white blood cells respond to organ damage, such as AKI. In my recently published work, I have been exploring treatment strategies to alter how STING works. I have moved to my supervisor's lab to build on this experience and examine how STING contributes to AKI in diabetes. To do this, I will perform experiments in unique models of AKI, the progression from AKI to CKD and AKI in diabetes. I am comparing what happens when we remove STING from all cells, just from kidney cells, or just from white blood cells. My hope is that these studies will lead to the development of a new treatment that improves kidney outcomes for people with diabetes, working by blocking the actions of STING.