In animal models, iron deficient mothers have a greatly increased risk of having offspring with congenital heart disease (CHD). The risk of CHD can be greatly reduced if the mother is given iron supplements very early in pregnancy. Additionally, embryos from a mouse model of Down Syndrome were particularly vulnerable to the effects of maternal iron deficiency, leading to a higher risk of developing severe heart defects.
A new study from the Parekh Group has resolved a long-standing question in our understanding of intracellular Ca2+ signalling, namely how a specific type of Ca2+ channel is uniquely able to signal to the nucleus to regulate gene expression. By unravelling this mechanism, researchers have identified a new approach for developing immunosuppressant drugs.
A new study from the Lakhal-Littleton Group has addressed a long-standing gap in our understanding of systemic iron homeostasis. It provides the first formal demonstration that the hormone hepcidin controls iron reabsorption in the kidney, in a manner that impacts the body’s iron levels, under normal physiological conditions. It also demonstrates for the first time how this mechanism becomes critically important in the development of iron disorders.