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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

Inflammation and immunity

• Medicine
• Surgery
• Anaesthetics
• Ophthalmology
• Paediatrics
• Pathology
• Public Health

• Adolescent medicine
• Cardiology
• Cardiac Surgery
• Dermatology
• Endocrinology
• Gastroenterology
• Geriatric Medicine
• Health Informatics
• Infectious diseases
• 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 in Chemistry, UCD 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. Our findings indicate potent, specific responses to these proprietary agents in the context of unresolved inflammation including atherosclerosis, CKD,sepsis and arthritis.

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.

Our interdisciplinary research lies at the interface of medicine, molecular biology, transcriptomics, genomics and bioinformatics. These integrated 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:

Primary Publications
• de Gaetano M et al., Asymmetric synthesis and biological evaluation of imidazole- and oxazole-containing synthetic lipoxin A4 mimetics (sLXms). Eur J Med Chem. 2019 Jan 15;162:80-108. doi: 10.1016/j.ejmech.2018.10.049. Epub 2018 Oct 23.PMID: 0419493
• Brennan EP et al., Lipoxins Protect Against Inflammation in Diabetes-Associated Atherosclerosis. Diabetes. 2018 Dec;67(12):2657-2667. doi: 10.2337/db17-1317
• van Zuydam NR et al., A Genome-Wide Association Study of Diabetic Kidney Disease in Subjects With Type 2 Diabetes. Diabetes. 2018 Jul;67(7):1414-1427. doi: 10.2337/db17-0914. Epub 2018 Apr 27.PMID: 29703844
• Brennan EP et al., Lipoxins Regulate the Egr-1 Network and Reverse Diabetic Kidney Disease J Am Soc Nephrol 2018 Feb 28. pii: ASN.2017101112
• Doody A, et al., Validating the association between plasma tumour necrosis factor receptor 1 levels and the presence of renal injury and functional decline in patients with Type 2 diabetes. J Diabetes Complications. 2018 Jan;32(1):95-99. doi: 10.1016/j.jdiacomp.2017.09.007. Epub 2017 Sep 18
• Bruen R et alLiraglutide dictates macrophage phenotype in apolipoprotein E null mice during early atherosclerosis. Cardiovasc Diabetol. 2017 Nov 6;16(1):143. doi: 10.1186/s12933-017-0626-3
• 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-β1-induced fibrotic responses in hypoxia and stabilises HIF-α 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 TGFβR1 J Am Soc Nephrol 2013, 24(4):627-37
• Borgeson 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-β1-Associated Gene Expression Profiles in Renal Epithelial Cells Reiterated in Human Diabetic Nephropathy. Biochim Biophys Acta. 2012;1822(4):589-5

Reviews
• Hughes MF et al., .Exploring Coronary Artery Disease GWAs Targets With Functional Links to Immunometabolism. Front Cardiovasc Med. 2018 Nov 6;5:148. doi: 10.3389/fcvm.2018.00148. PMID: 30460244
• Doyle R et al., Pro-resolving lipid mediators: Agents of anti-ageing? Semin Immunol. 2018 Dec;40:36-48. doi: 10.1016/j.smim.2018.09.002. PMID: 30293857
• Brennan EP et al., Specialized pro-resolving mediators in renal fibrosis. Mol Aspects Med. 2017 Dec;58:102-113
• Crean D et al., Specialised lipid mediators and their targets. Semin Immunol. 2015 May;27(3):169-76. doi: 10.1016/j.smim.2015.05.002
• Brazil DP et al., BMP signalling: agony and antagony in the family. Trends Cell Biol. 2015 May;25(5):249-264
• Manresa MC. et al., Hypoxia-sensitive pathways in inflammation-driven fibrosis. Am J Physiol Regul Integr Comp Physiol. 2014 Dec 15;307(12):R1369-80