Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we will assume that you are happy to receive all cookies and you will not see this message again. Click 'Find out more' for information on how to change your cookie settings.

Dr Samira Lakhal-Littleton

Dr Samira Lakhal-Littleton

My connections

Samira Lakhal-Littleton

BHF Intermediate Basic Science Research Fellow and University Research Lecturer

My research to date has revolved around metabolite homeostasis in cells and systems biology.  In recent years, I developed a more specialised interest in oxygen and iron homeostasis. In particular, I aim to understand how the significant interplay between oxygen and iron sensing pathways at the molecular level is reflected in the pathophysiology of human disease.

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 both oxygen and iron dependent, that I developed interest in iron and oxygen 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 two-year stint in the exciting field of exosome nanotechnology, I returned to the iron and oxygen field in 2012, and was awarded a four-year British Heart Foundation Intermediate Basic Science Research Fellowship.  My current work focuses on dissecting iron regulation in the heart, and determining the effects of altered cardiac iron metabolism on heart function and its responses to hypoxia, by utilising novel animal models of tissue-specific alterations in iron metabolism.

By gaining a mechanistic understanding of how iron is regulated at the single tissue level, and of its modulatory effect on responses to hypoxia, we can begin to explore the preventive or therapeutic potential of iron manipulation in diseases associated with pathophysiological responses to local or global hypoxia, e.g ischemic heart disease and pulmonary arterial hypertension.

False False

Key Publications


Recent Publications

20 View 2 more »