Grant: CIHR Fellowship

Diabetes is the most common cause of kidney failure across the globe. People with diabetes who develop kidney disease are much more likely to be admitted to hospital and they are much more likely to need access to healthcare as outpatients. Currently, the main treatments to stop kidney disease from getting worse in diabetes are medications that lower blood pressure or lower blood sugar levels. However, these treatments are only partly effective in limiting kidney damage. We urgently need new treatments for kidney disease in diabetes and we urgently need new ways of identifying people at risk of developing kidney disease. In my project, I will study how tiny molecules (called long non-coding RNAs) contribute to the kidney damage that happens in diabetes. RNAs are small molecules that pass the genetic code from the DNA in our cells to make proteins, the workhorses of the cells. Recently, scientists have discovered that a large amount of our DNA makes RNA that does not carry a code to make proteins. These RNA molecules are called small or long non-coding RNAs, based on their length. Although long non-coding RNAs do not carry a code to make proteins, they are important for how cells work. For example, they can help turn genes on or off or they can act as scaffolds to help other RNAs make proteins. We have recently discovered that the amount of a particular long non-coding RNA is increased in diabetic kidney disease and that blocking its actions helps protect kidney cells from damage caused by high sugar levels. In this project, I will conduct a series of experiments to explore the role of this long non-coding RNA in the development of diabetic kidney disease and to determine whether stopping this long non-coding RNA from working can protect against kidney damage. This could lead to the development of new treatments to help people with diabetic kidney disease and it could lead to new ways of identifying people with diabetes who are at risk of developing kidney disease.