Obesity causes damage to the kidney, a disease called obesity-related glomerulopathy (ORG). In normal health, protein is present in the blood from our diets and the kidney should only filter tiny amounts into the urine. Yet obese individuals often have large amounts of protein in urine (proteinuria) because the kidney's filtering units (glomeruli) are not working properly. Although proteinuria usually shows no or only mild symptoms, and therefore it can be easily missed, when long lasting proteinuria can lead to chronic kidney disease including diabetic nephropathy and kidney cancer.
The current treatments for ORG (e.g. weight loss and ramipril) are limited and often stop working over a period of time. Therefore, our research aims to understand how obesity damages kidney's filtering function and to develop a new way of improving kidney cells' way of working. This will help to develop new treatments for ORG and to prevent future chronic kidney disease.
We recently identified a novel pathway that controls kidney's function. Hyaluronan is a molecule in the network of molecules that surround cells, and CD44 and RHAMM are hyaluronan binding partners on the cell surface. When we removed hyaluronan, or CD44, or RHAMM in experimental models, obesity-related kidney damage was improved. However, it is unknown how this happens and whether we can target these molecules to develop therapies.
Insulin resistance, a condition where cells do not respond to the hormone insulin, is one of the reasons leading to ORG. Insulin acts in liver, muscle, and fat cells to lower the blood glucose level in the body. We have shown that removing hyaluronan or CD44 can reverse insulin resistance in these cells. It is recently recognised that insulin also acts directly in kidney cells and controls how kidney cells work. This led us to study whether insulin resistance in kidney cells causes kidney damage and whether we can restore kidney’s function by blocking the hyaluronan-CD44/RHAMM signalling in obesity.
This work will use both genetic and pharmacological approaches in vivo and in vitro to study kidney’s insulin responsiveness and its function in the context of obesity.
We can only fund Home fees. International students are welcome to apply but, if successful, must be able to fund the difference in fees.
Funding includes:
• Stipend - £18,700 - £19,800 per annum
• Tuition fees (UK rate only)
• Consumable costs (£10,000 per annum)
Start date: 4th September 2023
Informal enquiries please contact - Dr Li Kang - Email: [Email Address Removed]
To apply - please send your CV, a personal statement (up to 500 words), and transcripts if available to support your application to Dr Li Kang - Email: [Email Address Removed]
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