Professor Richard Coward
M.B.,Ch.B., Ph.D.(Bristol), M.R.C.P.
Current positions
Professor of Renal Medicine
Bristol Medical School (THS)
Contact
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Research interests
The Coward group study how the cells of the kidney function in health and in disease. They are particularly interested in examining how diabetes affects the cells of the kidney as this is the leading cause of kidney failure in the world requiring long-term dialysis or a kidney transplant. They also study a condition called Haemolytic Uraemic Syndrome (HUS) as this is the leading cause of rapid kidney failure in children needing dialysis in the UK, where it is associated with other severe complications including long-term kidney failure, brain damage and death in some children. Finally they have an interest in a debilitating inherited kidney stone disease called cystinuria which causes severe pain and can result in kidney failure.
Vision
To understand which of the cells in the kidney (there are over 20 different types) and signalling pathways that are crucial for maintaining kidney function and how they change, at a molecular level, when kidney disease develops.
Mission
The Coward group’s mission is to understand the important molecular pathways in cells the kidney that change in disease situations in order to develop better ways to prevent patients from developing kidney failure.
Approach
The group use a number of complementary techniques to identify the critical cells in the kidney that maintain its function and the key signalling pathways that keep them healthy. These include:
1. The development of kidney cell lines that can be studied outside the body in dishes. We have generated these from both man and mouse. A particular focus of our group is the podocyte cell which is crucial for preventing protein leaking into the urine (proteinuria). This cell is particularly important as proteinuria is predictive of long-term kidney failure and is also an independent risk factor for developing strokes or heart attacks. We are able to manipulate the signalling proteins in these cells by knocking them out or over expressing them so are able to work out key pathways that maintain the health of these cells.
2. Using mouse models, we are able to study cells of the kidney in their normal physiological setting when the kidneys are being perfused with blood and producing urine. Using Cre-lox technology we can specifically knockout or over-express key proteins in specific cell types to understand which specific cell signalling pathways are important in specific cell types.
3. Through an excellent collaboration with Dr Paul Hartley in Bournemouth University we have also studied the kidney of the fly to understand more about crucial signalling pathways that are evolutionarily conserved.
4. We also study large patient populations through superb world-wide collaborations. This includes being a part of the pan-European BEAt DKD project studying diabetic kidney disease.
Positions
University of Bristol positions
Professor of Renal Medicine
Bristol Medical School (THS)
Projects and supervisions
Research projects
Is Diabetic Nephropathy the Result of a Podocyte Tauopathy?
Principal Investigator
Managing organisational unit
Bristol Medical School (THS)Dates
01/08/2019 to 31/07/2022
Copy of Insulin signalling to the podocyte; pathological importance and therapeutic potential.
Principal Investigator
Managing organisational unit
Bristol Medical School (THS)Dates
01/08/2013 to 31/07/2019
MRC Award
Principal Investigator
Managing organisational unit
Bristol Medical School (THS)Dates
01/12/2006 to 01/12/2010
Thesis supervisions
Publications
Recent publications
14/08/2020Podocytes Produce and Secrete Functional Complement C3 and Complement Factor H
Frontiers in Immunology
An information theoretic approach to insulin sensing by human kidney podocytes
Molecular and Cellular Endocrinology
A role for NPY-NPY2R signaling in albuminuric kidney disease
Proceedings of the National Academy of Sciences of the United States of America
Modeling Podocyte Biology Using Drosophila Nephrocytes
Diabetic Nephropathy
Aldosterone induces albuminuria via matrix metalloproteinase–dependent damage of the endothelial glycocalyx
Kidney International