P1509: Bone Marrow Tfr2 Genetic Deletion Abrogates Blood Tranfusion Requirement in the Hbbth1/Th2 Β-Thalassemic Murine Model

Flavor of Iron at EHA2023: Novel Regulatory Mechanisms and Therapeutic Options for the Correction of Anemia

“…In line with this hypothesis, Dr Nai and colleagues demonstrated that mice lacking Tfr2 in the hematopoietic compartment showed reduced blood glycemia and improved glucose sensitivity both in a wild-type and in a β-thalassemic context, resulting also in a complete rescue of muscle functionality in β-thalassemic animals. 15 Blood glycemia negatively correlated with both red blood cells count and hemoglobin levels, supporting the concept that enhanced erythropoiesis drives increased glucose consumption. Overall, the presented data suggest that early metabolic alterations of β-thalassemic mice depend on the degree of ineffective erythropoiesis and are corrected by hematopoietic Tfr2 deletion that rewires systemic metabolism to sustain augmented erythropoiesis.…”

“…Thus, the authors postulated that the enhanced erythropoiesis induced by Tfr2 deletion, by stimulating the metabolic activity of erythroid cells, might prevent hyperglycemia and related complications in β‐thalassemia mice. In line with this hypothesis, Dr Nai and colleagues demonstrated that mice lacking Tfr2 in the hematopoietic compartment showed reduced blood glycemia and improved glucose sensitivity both in a wild‐type and in a β‐thalassemic context, resulting also in a complete rescue of muscle functionality in β‐thalassemic animals 15 . Blood glycemia negatively correlated with both red blood cells count and hemoglobin levels, supporting the concept that enhanced erythropoiesis drives increased glucose consumption.…”