Iron and pathophysiology: From basic mechanisms to clinical translation
our research
Unique biochemical properties underpin the essential functions of iron in oxygen transport and oxidative phosphorylation. Those same properties also underpin its propensity to participate in Fenton-type reactions, producing cell-damaging reactive oxygen species. Thus, tight control of iron levels within tissues is paramount for normal physiological function, particularly in tissues of high oxygen demand/flux.
Our research focusses on understanding the impact of too little or too much iron on the cardiovascular system, and on translating that understanding into better management of iron status in cardiovascular disorders.
For instance, iron deficiency is highly prevalent in the general population, and even more so in people with heart failure. Even in the absence of anaemia, iron deficiency increases the risk of incident heart failure and worsens outcomes in patients with existing heart failure. Consequently, iron supplementation, both oral and intravenous have become embedded in clinical guidelines for the management of iron deficiency in cardiovascular settings. In our team, we aim to:
1) identify the pathways that drive iron deficiency in chronic disorders
2) understand, at the mechanistic level, the impact of iron deficiency on cardiac adaptations to stress in different settings, e.g. heart failure, heart attack, pregnancy
3) determine whether myocardial iron levels are relevant to the above
4) develop new non-invasive biomarkers of myocardial iron levels
5) examine the impact of different iron supplementation approaches on myocardial iron and myocardial responses to stress
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