Associate Professor of Cell Physiology and MRC Senior Non-Clinical Research Fellow
- Principal Investigator
- Tutorial Fellow in Medicine Brasenose College Oxford
My research to date has revolved around nutrient homeostasis in cells and systems biology. In recent years, I developed a more specialised interest in iron homeostasis. In particular, I aim to understand how iron is controlled in various systems and the importance of such control for normal physiological function.
Following a degree in Human Genetics at University College London, I joined the University of Oxford in 2004 as a DPhil student in the laboratory of Prof Cerundolo at the Weatherall Institute of Molecular Medicine. At the time, I was interested in the role of amino acid metabolism in the regulation of immune responses and tumour immune surveillance. It was during that time, while working on a tryptophan-degrading enzyme that is iron-dependent, that I developed interest in iron homeostasis.
In 2007, I went on to undertake my first postdoctoral project in the laboratory of Prof Ratcliffe, focussing on the interplay between Hypoxia Inducible Factors (HIFs) and iron homeostasis. HIFs, master transcription factors whose function is regulated by both oxygen and iron levels, in turn regulate cellular and systemic iron levels. My research findings defined some of the molecular mechanisms underlying the relationship between HIFs, hypoxia and iron homeostasis, e.g I discovered that the iron regulatory genes TMPRSS6 and GDF15 are both responsive to hypoxia. I also collaborated with human physiologists in a bid to understand how the major iron regulatory hormone hepcidin is regulated by altitude hypoxia and iron status. TMPRSS6, GDF15 and Hepcidin are all implicated in diseases of deregulated iron metabolism.
Following a period of maternity leave, I returned to the iron and oxygen field in 2012, and was awarded a four-year British Heart Foundation Intermediate Basic Science Research Fellowship. In 2019, I was elected to the Board of Directors of the Internal BioIron Society. My current work focuses on dissecting iron regulation in the heart, the kidney, the placenta and the vasculature, by utilising novel animal models of tissue-specific alterations in iron metabolism.
In 2020, I was awarded an MRC Senior Non-Clinical Research Fellowship, to address the clinical implications of local iron control in the setting of chronic heart failure.
Minimal effect of conditional ferroportin KO in the neural retina implicates ferrous iron in retinal iron overload and degeneration.
Liu Y. et al, (2022), Exp Eye Res, 218
The kidney hepcidin/ferroportin axis controls iron reabsorption and determines the magnitude of kidney and systemic iron overload.
Mohammad G. et al, (2021), Kidney Int, 100, 559 - 569
Fetal liver hepcidin secures iron stores in utero.
Kämmerer L. et al, (2020), Blood, 136, 1549 - 1557
Dendritic cell-derived hepcidin sequesters iron from the microbiota to promote mucosal healing.
Bessman NJ. et al, (2020), Science, 368, 186 - 189
Ferroportin-mediated iron export from vascular endothelial cells in retina and brain.
Baumann BH. et al, (2019), Exp Eye Res, 187
Liver-Specific, but Not Retina-Specific, Hepcidin Knockout Causes Retinal Iron Accumulation and Degeneration.
Baumann BH. et al, (2019), Am J Pathol, 189, 1814 - 1830
Iron Deficiency as a Therapeutic Target in Cardiovascular Disease.
Lakhal-Littleton S., (2019), Pharmaceuticals (Basel), 12
IMPACTS OF MATERNAL IRON DEFICIENCY ON THE MOUSE PLACENTAL-HEART AXIS
Kalisch-Smith J. et al, (2019), PLACENTA, 83, E47 - E48