Inhibition of FGF23 Is a Therapeutic Strategy to Target Hematopoietic Stem Cell Niche Defects in β-Thalassemia

Researchers demonstrated that fibroblast growth factor 23 (FGF23) was increased in patients and mice with β-thalassemia because erythropoietin induced FGF23 overproduction in bone and bone marrow erythroid cells via ERK1/2 and STAT5 pathways.