NIH R01 · 2025
Pathological consequences of iron excess and hypoxia in β-thalassemia pregnancy
PROJECT SUMMARY Excess redox-active iron, and consequent oxidative stress, contribute to the morbidity and mortality associated with β-thalassemia. Iron overload develops due to low hepcidin and excessive intestinal iron absorption, and from blood transfusions. Anemia and tissue hypoxia, due to ineffective erythropoiesis, also typify β-thalassemia. Pregnancy in β-thalassemia is becoming more common but is considered high risk. The relative contributions of iron overload/oxidative stress and anemia/hypoxia to adverse fetal outcomes are, however, unknown. Given this gap in clinical knowledge, investigation in this area of scientific pursuit is warranted. We utilized a pre-clinical model of…
From the public funding record at NIH RePORTER. Describes the funded project, not the reviews below.