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New therapeutic targets in diabetic kidney disease. A role of GDF-15?

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Title:  New therapeutic targets in diabetic kidney disease. A role of GDF-15?
Investigator:  A Bidadkosh
Promotor: RH Henning
Co-promoter(es):  LE Deelman, JH Buikema
Summary:  Type 2 diabetes is quickly becoming a disease of epidemic proportions and despite glycaemic control, diabetic nephropathy remains a common and serious complication of diabetes. Intervention in earlier stages of diabetic renal disease, when overt nephropathy is not yet present, appears to be superior as compared to late intervention. Thus, new strategies aiming at early detection and treatment of kidney disease, before functional and/or structural damage is present, may hold promise to further delay the progression of diabetic nephropathy on top of current established therapies.

Studies in early experimental diabetes identified growth differentiation factor 15 (GDF15) as a factor that is upregulated immediately after induction of diabetes. Further, mice that were genetically deleted for GDF15 demonstrated enhanced tubular damage in diabetes, indicating that GDF15 is a protective factor for the kidney. In a translational approach we have further demonstrated that GDF15 predicts for the progression of type 2 diabetes in patients, demonstrating that GDF15 may become an important biomarker for disease progression. Taken together, our studies demonstrate that GDF15 may become an important new tool for detection and treatment of diabetic kidney disease.

Our current line of research focuses on the identification of drugs that modulate GDF15 levels in both patients and animals. New advanced genetic models are being developed to further investigate the role of GDF15 in diabetes. Finally, the involvement of GDF15 in disease progression is extended to obesity induced diabetes, hypertension and hyperlipidemia collectively known as metabolic syndrome.

Financing:  Tasman bursary
Start:  1-03-2014
End:  1-03-2016

Projects
Organ damage and the role of CBS in hibernation.
Mechanisms and modulation of the immune response in sterile sepsis.
The CBS/H2S pathway in the brain.
Platelet dynamics in natural and pharmacologically induced hibernation.
Liver fibrosis and hibernation.
Towards prevention of neuroinflammation in major surgery.
Limiting the impact of stroke.
Identification of kinomic key proteins involved in tachycardia and stretch induced cardiomyocyte remodeling.
Role of epigenetic regulation by histone acetylation in the induction of Atrial Fibrillation.
Reversal of cardiomyocyte remodeling in Atrial Fibrillation; the role of protein degradation and translation modulators.
REVersal of cardiomyocyte structural remodeling and Improvement of functional recoVEry in Atrial Fibrillation: REVIVE.
HSF1 Activators Lower cardiomyocyte damage: towards a novel Therapeutic approach to REVERSE Atrial Fibrillation. HALT&REVERSE
Mutations in HSPB5, HSPB7 and BAG3 lead to juvenile DCM.
New therapeutic targets in diabetic kidney disease. A role of GDF-15?
Role of cyclooxygenase signalling on vascular dysfunction in the metabolic syndrome.
Vascular (Dys-)Function as a Determinant of Susceptibility to Diabetic Nephropathy: a Focus on Myogenic Constriction.