A team from the University of Lincoln has been awarded 80,000 Euros to develop research to help improve understanding of the leading cause of end-stage kidney disease in diabetes patients.
The European Federation for the Study of Diabetes has awarded the Janssen Kidney Award to Dr Claire Hills and Professor Paul Squires, whose joint research aims to better understand the sub-cellular mechanisms that regulate how people with diabetes can end up with diabetic nephropathy (kidney disease).
As the leading cause of end-stage kidney disease, diabetic nephropathy is a debilitating and potentially life threatening complication of diabetes.
Every cell in the body is surrounded by a complex matrix of proteins that allows them to interact with each other and their immediate environment.
This extracellular matrix allows cells to detect survival signals in times of stress and has a crucial role in maintaining appropriate cell function. Changes to the matrix have been linked to a number of diseases, such as diabetes.
In the current study, Dr Hills and Professor Squires will examine how glucose and associated cytokines (small proteins that are important in cell signalling) reduce ‘stickiness’ between neighbouring cells of the proximal kidney and between cells and their surrounding matrix.
Dr Hills said: “Little is known about the mechanisms through which these glucose-induced detrimental effects occur, however, we believe that a loss of these interactions changes the behaviour of cells and contributes to the high level of damage seen in diabetes.”
With the help of international collaborators, biopsy material from both healthy kidneys and those obtained from patients with diabetic nephropathy will ensure that work accurately models the situation in humans.
Dr Hills added: “To identify future therapeutic targets in our fight against the increasing prevalence of this condition, we need to understand the basic mechanisms that prevent kidney cells from functioning correctly.”
The research will improve understanding of why renal function is often impaired in diabetes and will identify pathways that may alleviate and/or prevent glucose-induced damage of normal kidney function.
For additional information please see: http://www.europeandiabetesfoundation.org/index.php/ct-menu-item-9/14-sample-data-articles/173-recipient