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• genetics, genomics and molecular biology
• infectious disease and the immune system
• cell and developmental biology/regenerative medicine
• physiology and non-communicable disease
• Other - please suggest keyword(s):

• Medicine
• Surgery
• Ophthalmology
• Pathology
• Public Health

• Adolescent medicine
• Cardiology
• Cardiac Surgery
• Endocrinology
• Gastroenterology
• Geriatric Medicine
• Health Informatics
• Immunology
• Nephrology
• Pharmacology
• Respiratory Medicine
• Rheumatology
• Vascular Medicine

Work in my group focuses on the molecular mechanisms underlying the initiation, progression and potential regression of microvascular complications of diabetes. We have a particular interest in the resolution of inflammation and how this may be subverted in numerous prevalent diseases. We have identified a role for endogenously generated lipid mediators [lipoxins, LXs] in promoting the resolution of inflammation. Working in collaboration with Prof Pat Guiry's group we have generated a series of novel synthetic mimetics of LX bioactions. We are currently characterising the bioactions of these molecules in in vitro and in vivo model systems and human tissue ex vivo. We are part of an international consortium investigating the genetic susceptibility to diabetic kidney disease. Together with investigators at The Broad Institute of Harvard and MIT, QUB and The University of Helsinki we have identified several novel genes implicated in diabetic kidney disease. Our efforts are focused on understanding how these genetic variants may contribute to disease susceptibility and or resistance with a view to developing therapeutic interventions and or dynamic biomarkers of susceptibility and disease progression. Interestingly many of the genetic variants implicated are associated with inflammatory processes. The team comprises basic scientists, clinician investigators and bioinformaticians. We are part of the multidisciplinary Diabetes Complications Research Centre at UCD
Sample Publications cf below.

Our interdisciplinary research lies at the interface of medicine, molecular biology, transcriptomics, genomics and bioinformatics. These intergrated approaches will realise the potential for understanding the pathogenesis of disease and by extension the development of novel diagnostics and therapeutics. Researchers work as part of a bigger group in The Diabetes Complications Research Centre [DCRC]at The Conway and with collaborators at clinical sites including MMUH, SVUH and Beaumont Hospital. Active collaborations are ongoing with Prof Peter Maxwell [QUB], Drs Hirschhorn and Jose Florez [Harvard and MIT] and Professor Mauro Perretti [London]. DCRC Principal Investigators include Prof Carel Le Roux, Prof Helen Roche, Prof Donal O?Shea, Dr Orina Belton, Dr John Crean] providing a critical interdisciplinary mass of investigators and a vibrant research culture. The Conway Institute is a state of the art biomedical research institute committed to translational research. The technological infrastructure and intellectual resources at the Conway are excellent and support high quality, ambitious research. Investigations in the Godson lab are supported by Science Foundation Ireland, NIH, JDRF, HRB, Wellcome Trust and the EU. Sample projects are indicated below however any PhD project would be specifically tailored to the expertise and ambition of the candidate to ensure an optimal outcome. We have a long tradition of training PhD clinician scientists most of whom remain in academic medicine in Ireland, the UK or US.
Sample Projects:
Novel transcriptomic networks analysis in CKD
Pro resolution mimetics: characterisation and biological activity in in vitro, in vivo and human tissue ex vivo
Innate immune responses underlying the initiation, progression and potential regression of in obesity and associated complications
Design and Characterisation of novel TGF-b super-family agonists and antagonists as modulators of fibrotic disease.

Recent Sample Publications:
Reviews
? Crean et al., Specialised lipid mediators and their targets. Semin Immunol. 2015 May;27(3):169-76
? Brazil et al., BMP signalling: agony and antagony in the family. Trends Cell Biol. 2015 May;25(5):249-264
? Maderna P and Godson C Lipoxins: Resolutionary Road, Br. J. Pharmacol. 2009 8:947-59
Primary Publications
? Cavadas et al., REST is a hypoxia-inducible repressor of transcription Sci Reports 2016 Aug 17;6:31355
? Wang et al., Mesenchymal stem cells deliver exogenous microRNA let7c via exosomes to attenuate renal fibrosis Mol. Ther. 2016 in press
? Beaton et al., Wnt6 regulates epithelial cell differentiation and is dysregulated in renal fibrosis.Am J Physiol Renal Physiol. 2016 Apr 27
? Todd et al., Genetic Evidence for a Causal Role of Obesity in Diabetic Kidney Disease. Diabetes. 2015 Dec;64(12):4238-46
? Borgeson et al., Lipoxin A4 attenuates obesity-induced adipose inflammation and associated liver and kidney disease.Cell Metab. 2015 Jul 7;22(1):125-3
? Locke AE, Genetic studies of body mass index yield new insights for obesity biology Nature. 2015 Feb 12;518(7538):197-206
? Shungin D New genetic loci link adipose and insulin biology to body fat distribution. Nature. 2015 Feb 12;518(7538):187-96.
? Nolan et al., Paricalcitol protects against TGF-?1-induced fibrotic responses in hypoxia and stabilises HIF-? in renal epithelia. Exp Cell Res. 2015 Jan 15;330(2):371-81.
? Hickey et al., IHG-1 increases mitochondrial fusion and bioenergetic function. Diabetes. 2014 Dec;63(12):4314-25
? Brennan et al., Lipoxins attenuate renal fibrosis by induction of let-7c and suppression of TGF?R1 J Am Soc Nephrol 2013, 24(4):627-37.
? B?rgeson et al.,Lipoxin A4 attenuates adipose inflammation. FASEB J. 2012 , Oct;26(10):4287-94.
? Sandholm, N et al., * New Susceptibility Loci Associated with Kidney Disease in Type 1 Diabetes. PLoS Genet. 2012 Sep;8(9):e100292
? Brennan er al., Next-Generation Sequencing Identifies TGF-?1-Associated Gene Expression Profiles in Renal Epithelial Cells Reiterated in Human Diabetic Nephropathy Biochim Biophys Acta. 2012;1822(4):589-599