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The TGF-β superfamily comprises multifunctional signaling proteins and key regulators of homeostasis and repair throughout the body.1 Dysfunction of TGF-β superfamily members has been implicated in cancer and other pathological conditions. Ligands in this superfamily mediate their diverse effects by inducing distinct combinations of type I and II receptors and their downstream effectors—Smad proteins.1
Preclinical studies have shown that Smad2/3 signaling, mediated by members of the TGF-β superfamily, may have effects on erythroid precursors2-4 and is involved in regulating late-stage erythropoiesis.5-7 Defective late-stage erythropoiesis results in impaired red blood cell maturation, leading to anemia and contributing to iron overload.8,9 However, the specific roles of Smad2/3 signaling in red blood cell production have not been fully elucidated. In a mouse model of β-thalassemia, inhibition of abnormally elevated Smad2/3 signaling improved hematology parameters associated with ineffective erythropoiesis.10