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Relevant bibliographies by topics / Erythropoietin receptor, Thalassemia, Hemoglobin, Parkinson's disease / Journal articles

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Journal articles on the topic 'Erythropoietin receptor, Thalassemia, Hemoglobin, Parkinson's disease'

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Published: 14 March 2023

Last updated: 31 July 2025

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1

Galanello, R., S. Barella, MP Turco, et al. "Serum erythropoietin and erythropoiesis in high- and low-fetal hemoglobin beta-thalassemia intermedia patients." Blood 83, no. 2 (1994): 561–65. http://dx.doi.org/10.1182/blood.v83.2.561.561.

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Abstract Clinical data suggest that in beta-thalassemia-intermedia patients, higher levels of circulating fetal hemoglobin (HbF) are associated with greater disease severity at comparable degrees of anemia. We assessed the influence of the amount of circulating HbF on serum erythropoietin (s-Epo) levels and on serum transferrin receptor, a measure of erythropoiesis, in 30 beta-thalassemia-intermedia patients. Twenty-four showed more than 40% HbF (21 of whom with beta (0)-thalassemia) and 6 presented lower HbF levels (beta(+)-thalassemia). The two groups of patients did not differ in age (15.3

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2

Galanello, R., S. Barella, MP Turco, et al. "Serum erythropoietin and erythropoiesis in high- and low-fetal hemoglobin beta-thalassemia intermedia patients." Blood 83, no. 2 (1994): 561–65. http://dx.doi.org/10.1182/blood.v83.2.561.bloodjournal832561.

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Clinical data suggest that in beta-thalassemia-intermedia patients, higher levels of circulating fetal hemoglobin (HbF) are associated with greater disease severity at comparable degrees of anemia. We assessed the influence of the amount of circulating HbF on serum erythropoietin (s-Epo) levels and on serum transferrin receptor, a measure of erythropoiesis, in 30 beta-thalassemia-intermedia patients. Twenty-four showed more than 40% HbF (21 of whom with beta (0)-thalassemia) and 6 presented lower HbF levels (beta(+)-thalassemia). The two groups of patients did not differ in age (15.3 v 19 year

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3

Fibach, Eitan, and Johnny Amer. "The In Vitro and In Vivo Antioxidant Effects of Erythropoietin in Thalassemia." Blood 110, no. 11 (2007): 573. http://dx.doi.org/10.1182/blood.v110.11.573.573.

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Abstract Erythropoietin (EPO), a hormone produced on hypoxia mainly in the kidneys, enhances red blood cell (RBC) production (erythropoiesis) by stimulating the proliferation of erythroid progenitors and precursors in the bone marrow. This effect is mediated by the homodimeric EPO receptor, a class 1 cytokine receptor. Recombinant human EPO is widely used for the treatment of anemia, e.g., in patients on dialysis, patients with myelodysplastic syndrome and oncology patients undergoing chemotherapy. Treatment with EPO was also tried experimentally in patients with thalassemia. In these patients

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4

Mahagna, Lila, Osama Tanous, Tal Dujovny та ін. "Leptin Is Associated with the Degree of Anemia and the Erythropoietin Levels in β Thalassemia Patients". Blood 130, Suppl_1 (2017): 950. http://dx.doi.org/10.1182/blood.v130.suppl_1.950.950.

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Abstract Background: β-thalassemia (BT) is a hereditary hemolytic anemia. The imbalance between α- and β-globin chain synthesis results in ineffective erythropoiesis, severe microcytic hypochromic anemia and iron overload. Although regular transfusions and iron-chelation therapy markedly improve the survival and quality of life of BT patients, they have also led to the emergence of previously unrecognized complications. Patients with thalassemia major often present with endocrine abnormalities due to dysfunction of the hypothalamic-pituitary axis (Poggi, 2016), and are frequently underweight w

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Lob, Heinrich E., Leah Kravets, Lawrence Miloscio, Jason Mastaitis, Aris N. Economides та Sarah J. Hatsell. "Anti-GDF11Treatment of β-Thalassemia Intermedia Mice Does Not Improve Erythropoiesis". Blood 136, Supplement 1 (2020): 7–8. http://dx.doi.org/10.1182/blood-2020-140605.

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Beta-thalassemia is a hereditary iron-independent anemia, caused by a reduction of β-globin, affecting millions of people globally. Current treatments such as blood transfusions and iron chelation show significant toxicities and add to organ damage. Luspatercept (Acvr2b(L79D)-Fc) is a novel treatment for transfusion-dependent β-thalassemia patients that improves erythropoiesis independent of erythropoietin. The exact mechanism of action remains unknown, and it is controversially discussed if growth differentiation factor 11 (GDF11) is the main target of this drug. Genetic models raised doubts

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Chu, Simon N., Eric Soupene, Beeke Wienert та ін. "Dual α-Globin and Truncated EPO Receptor Knockin Restores Hemoglobin Production in α-Thalassemia-Derived Hematopoietic Stem and Progenitor Cells". Blood 142, Supplement 1 (2023): 485. http://dx.doi.org/10.1182/blood-2023-180187.

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Introduction: α-thalassemia major (ATM) is an autosomal recessive disorder where all four copies of the α-globin gene are deleted. A traditionally lethal disease due to severe fetal hypoxia, this condition is now survivable due to the advent of in utero blood transfusions. However, patients still require life-long transfusions postnatally. While allogeneic hematopoietic stem cell transplant (HSCT) can provide a definitive cure, it is limited by the paucity of suitable donors, has a high morbidity and mortality due the prerequisite myeloablative regimens, and carries the risk of immune rejectio

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7

Cazzola, M., L. Ponchio, F. de Benedetti, et al. "Defective iron supply for erythropoiesis and adequate endogenous erythropoietin production in the anemia associated with systemic-onset juvenile chronic arthritis." Blood 87, no. 11 (1996): 4824–30. http://dx.doi.org/10.1182/blood.v87.11.4824.bloodjournal87114824.

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Systemic-onset juvenile chronic arthritis (SoJCA) is associated with high levels of circulating interleukin-6 (IL-6) and is frequently complicated by severe microcytic anemia whose pathogenesis is unclear. Therefore, we studied 20 consecutive SoJCA patients with hemoglobin (Hb) levels <12 g/dL, evaluating erythroid progenitor proliferation, endogenous erythropoietin production, body iron status, and iron supply for erythropoiesis. Hb concentrations ranged from 6.5 to 11.9 g/dL. Hb level was directly related to mean corpuscular volume (r = .82, P < .001) and inversely related to circulati

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8

Casu, Carla, Pedro Ramos, Luca Melchiori, et al. "Potential Therapeutic Applications of Jak2 Inhibitors in Beta-Thalassemia and Sickle Cell Disease,." Blood 118, no. 21 (2011): 3187. http://dx.doi.org/10.1182/blood.v118.21.3187.3187.

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Abstract Abstract 3187 ß-Thalassemia and sickle cell disease (SCD) are the most common genetic red blood cell (RBC) disorders characterized respectively by limited production of aberrant ß-globin chains. In both cases, chronic transfusions and iron chelation are required to treat the anemia and/or formation of abnormal RBC. In ß-thalassemia, anemia stimulates erythropoietin (Epo) synthesis, which in turn leads to increased erythropoiesis and development of hepatosplenomegaly, often resulting in the need for splenectomy. Recently, we demonstrated that erythroid cells from ß-thalassemic mice hav

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9

Guerrero, Manuel Ugidos, Sujit Sheth, Olivier Hermine та Sadanand Vodala. "Improvement of Underlying Disease Pathophysiology of Ineffective Erythropoiesis in Non-Transfusion-Dependent (NTD) Patients with β-Thalassemia Receiving Luspatercept: Biomarker Analysis from the BEYOND Trial". Blood 142, Supplement 1 (2023): 1104. http://dx.doi.org/10.1182/blood-2023-179122.

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Background: Ineffective erythropoiesis and chronic hemolytic anemia are hallmarks of β-thalassemia which ultimately lead to extramedullary hematopoiesis (EMH), iron overload and other complications. Patients with hemoglobin levels chronically &lt; 10 g/dL are at higher risk for clinical complications and mortality. A significant proportion of patients treated with luspatercept on the BEYOND study (NCT03342404) achieved ≥ 1.0 g/dL hemoglobin increases from baseline, with a manageable safety profile. This increase of hemoglobin is associated with improvement in health-related quality of life

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Di Modica, Simona Maria, Emanuele Tanzi, Alessia Pagani, Laura Silvestri та Antonella Nai. "Hyperactive Erythropoiesis Induced By Hematopoietic Tfr2 Deletion Corrects Glucose Abnormalities in β-Thalassemic Mice". Blood 144, Supplement 1 (2024): 3852. https://doi.org/10.1182/blood-2024-207290.

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Introduction: β-thalassemia is a genetic disease characterized by anemia, ineffective erythropoiesis and iron-overload due to inadequate hemoglobin production, which leads to premature cell death. Alterations of glucose metabolism and diabetes are common complications of the disease, usually ascribed to organ dysfunction because of iron accumulation. However, β-thalassemia carriers, who do not present iron-overload, have a higher risk of developing diabetes compared to the general population, suggesting that factors other than iron may contribute to glycometabolic abnormalities. Transferrin Re

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11

Tamary, Hannah, Joseph Kapelushnik, Galit Perez-Avraham, Itai Levi, Carole Brasse-Lagnel, and Hanna Shalev. "High Levels of Soluble Serum Hemojuvelin in Patients with Congenital Dyserythropoietic Anemia Type I,." Blood 118, no. 21 (2011): 3179. http://dx.doi.org/10.1182/blood.v118.21.3179.3179.

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Abstract Abstract 3179 Ineffective erythropoiesis in congenital dyserythropoietic anemia type I (CDA I) is characterized by increased iron absorption mediated by down-regulation of hepcidin. It has been suggested that growth differentiation factor 15 (GDF15) contributes to the inappropriate suppression of hepcidin. Hemojuvelin (HJV), an important regulator of hepcidin production, is highly expressed in skeletal muscle and the liver. Mutations in the gene encoding HJV lead to severe hepcidin deficiency and juvenile hemochromatosis. Membrane-bound HJV (m-HJV) acts as a co-receptor for bone morph

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12

Yee, Andrew J., Jacob P. Laubach, Ajay K. Nooka, et al. "Phase 1 Dose-Escalation Study of Sotatercept (ACE-011) in Combination with Lenalidomide and Dexamethasone in Patients with Relapsed and/or Refractory Multiple Myeloma." Blood 126, no. 23 (2015): 4241. http://dx.doi.org/10.1182/blood.v126.23.4241.4241.

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Abstract Introduction Anemia and bone disease are hallmarks of multiple myeloma (MM). Sotatercept (ACE-011) is a novel, first-in-class activin type IIA receptor fusion protein that binds with high affinity to activin A and GDF11, and it acts during late-stage erythropoiesis to increase the production of mature erythrocytes through a mechanism independent of erythropoietin. Sotatercept has shown promising activity in clinical trials for anemia in myelodysplastic syndromes (Komrokji et al., ASH 2014) and in thalassemia (Cappellini et al., EHA 2015). Additionally, we have shown that targeting act

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13

Schmidt, Paul J., Anoop K. Sendamarai, Ivanka Toudjarska та ін. "RNAi-Mediated Inhibition of Tmprss6 Ameliorates Anemia and Secondary Iron Overload in a Mouse Model of β-Thalassemia Intermedia and Decreases Iron Overload in Hfe−/− Mice". Blood 120, № 21 (2012): 1018. http://dx.doi.org/10.1182/blood.v120.21.1018.1018.

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Abstract Abstract 1018 β-Thalassemia intermedia (TI), an inherited hemoglobinopathy caused by partial loss of β-globin synthesis, is characterized by anemia, extramedullary hematopoiesis and ineffective erythropoiesis as well as secondary iron overload. Hereditary hemochromatosis (HH) is most frequently caused by mutations in HFE and is marked by excess uptake of dietary iron with concomitant tissue iron overload. In both diseases, increased iron absorption is due to inappropriately low levels of the liver hormone, hepcidin (encoded by Hamp1). The membrane serine protease Matriptase-2 (encoded

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14

Luna, Sofia E., Joab Camarena, Jessica P. Hampton, et al. "Using Human Genetics to Develop Strategies to Increase Erythropoietic Output from Genome-Edited Hematopoietic Stem and Progenitor Cells." Blood 142, Supplement 1 (2023): 5003. http://dx.doi.org/10.1182/blood-2023-174170.

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Genome editing is a powerful tool that enables precise changes in the genetic code of a cell. Genome-edited hematopoietic stem and progenitor cells (HSPCs) yield genome-corrected cells of all lineages, yet the only cell type of clinical relevance in red blood cell (RBC) disorders is the RBC. Most applications of genome editing have sought to correct disease-causing mutations of monogenic diseases. However, human genetic variation reveals variants that confer positive health benefits as well. In this study we took advantage of a naturally occurring human variant to increase erythropoietic outpu

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15

Zhang, Xin, Valentina D'Escamard, Pauline Rimmele, and Saghi Ghaffari. "Regulation of Erythroid Cell Maturation Is Mediated by a Foxo3-mTOR Cross Talk: Outcome for Beta-Thalassemic Erythropoiesis." Blood 118, no. 21 (2011): 176. http://dx.doi.org/10.1182/blood.v118.21.176.176.

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Abstract Abstract 176 Differentiation of erythroid progenitors to mature red blood cells requires erythropoietin receptor (EpoR) signaling. Stimulation of EpoR results in Jak2-mediated activation of mainly AKT, ERK/MAPK and STAT5 signaling pathways. Although alteration of these pathways is involved with the pathophysiology of major erythroid disorders such as beta-thalassemia mechanisms by which these signals impact transcriptional programs of erythroid cell maturation are largely unknown. We have shown previously that AKT signaling is required for Epo-mediated erythroid cell maturation and id

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16

Di Modica, Simona Maria, Violante Olivari, Emanuele Tanzi та ін. "Tfr2 Genetic Deletion Makes Transfusion-Independent a Murine Model of Transfusion-Dependent β-Thalassemia". Blood 138, Supplement 1 (2021): 575. http://dx.doi.org/10.1182/blood-2021-148419.

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Abstract β-thalassemia is an autosomal recessive disorder due to mutations in the β-globin gene, that leads to defective production of hemoglobin (Hb) and red blood cells (RBC). The main features of the disease are anemia, ineffective erythropoiesis and iron overload. Patients affected by the most severe form of β-thalassemia are transfusion-dependent (TDT) and require lifelong blood transfusions and iron chelation, symptomatic treatments that affect the quality of life. The only curative option, unfortunately limited by the insufficient number of HLA-matched donors, is allogenic bone marrow (

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17

Oikonomidou, Paraskevi Rea, Ping La, Ritama Gupta та ін. "Genetic Investigation of the Role of GDF11 in the Treatment of β-Thalassemia and MDS". Blood 128, № 22 (2016): 2439. http://dx.doi.org/10.1182/blood.v128.22.2439.2439.

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Abstract The current treatment of β-thalassemia only partially mitigates the phenotype of the disease, making the need for novel therapeutic agents imperative. The investigational drug Luspatercept (ACE-536) is a ligand trap that contains the modified extracellular domain of activin receptor IIB (ACVR2B) and induces red blood cell production in an erythropoietin independent fashion. ACE-536 binds with high affinity to members of the transforming growth factor (TGF) β superfamily and therefore alters activin/GDF signaling through the intracellular SMAD complex. In search of the specific ligands

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18

Olivari, Violante, Maria Rosa Lidonnici, Mariam Aghajan, et al. "Rebalancing Iron Homeostasis and Erythropoiesis through Tfr2 Inhibition for Correction of Anemia in CKD." Blood 138, Supplement 1 (2021): 940. http://dx.doi.org/10.1182/blood-2021-148384.

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Abstract Background Transferrin Receptor 2 (TFR2) is a protein expressed in the liver and in the erythroid compartment. Hepatic TFR2 activates the transcription of hepcidin, the master regulator of iron homeostasis, and its inactivation causes iron overload. Erythroid TFR2 interacts with Erythropoietin (EPO) receptor and its deletion enhances erythropoiesis increasing EPO sensitivity of erythroid cells. We recently demonstrated that bone marrow (BM) Tfr2 loss improves anemia in a murine model of β-thalassemia. We hypothesized that the same approach might represent a therapeutic option also for

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