Growth differentiation factor 15 in erythroid health and disease
Open accessAbstract
PURPOSE OF REVIEW: Growth differentiation factor 15 (GDF15) was identified as a hepcidin-suppression factor that is expressed at high levels in patients with ineffective erythropoiesis. This review addresses the regulation, expression and potential functions of GDF15 in the context of erythroid biology. RECENT FINDINGS: GDF15 expression during late erythroid differentiation was discovered as part of an erythroblast transcriptome project. As GDF15 expression is associated with cellular stress or apoptosis, further investigation of the cytokine was focused upon its involvement in ineffective erythropoiesis. Remarkably high serum levels were detected in patients with thalassemia syndromes, congenital dyserythropoiesis and some acquired sideroblastic anemias. High-level GDF15 expression is not a feature of normal erythropoiesis, or erythroid recovery after bone-marrow transplantation. As GDF15 is a transforming growth factor-beta superfamily member, it was investigated as an effector of ineffective erythropoiesis that suppresses hepcidin expression despite iron overloading. SUMMARY: In contrast to the low levels of GDF15 expressed during normal erythropoiesis, ineffective erythropoiesis causes high-level expression of GDF15. In patients with thalassemia and related anemias, GDF15 expression may contribute to iron overloading or other features of the disease phenotype.
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Increased GDF15 serum levels associate with syndromes of ineffective erythropoiesis, for example α- and β-thalassemia.
“While increased GDF15 serum levels associate with syndromes of ineffective erythropoiesis, for example α- and β-thalassemia”
From Regulation of erythropoiesis by hypoxia-inducible factors (2013) · cites this paper as [216]
GDF-15 and TWSG1 are candidate erythrokines, although not erythroblast-specific, that have the potential to suppress hepcidin under conditions of increased erythropoietic activity.
“Growth differentiation factor 15 (GDF-15) and twisted gastrulation homolog 1 (TWSG1) have been identified as candidate erythrokines, although not erythroblast-specific, that have the potential to suppress hepcidin under conditions of increased erythropoietic activity.”
From Regulation of erythropoiesis by hypoxia-inducible factors (2013) · cites this paper as [216]
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- Authors
- Tanno, T., Noel, P., & Miller, J. L.
- Affiliations
- National Institutes of Health (US)
- Venue
- Current Opinion in Hematology
- Published
- 2010-02
- Volume
- 17
- Issue
- 3
- Pages
- 1
- ISSN
- 1065-6251 (ISSN-L)
- PMC
- PMC2884377
- OpenAlex
- W2128706348
- Cited by
- 139
- References
- 10
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 9 · 2023: 9 · 2022: 9 · 2021: 10 · 2020: 9 · 2019: 11 · 2018: 2 · 2017: 7 · 2016: 10 · 2015: 11 · 2014: 15 · 2013: 10 · 2012: 10
- FWCI
- 7.59
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Current Opinion in Hematology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (Z01DK025100)
- Topics
- Health Sciences › Medicine › Rheumatology › GDF15 and Related Biomarkers
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Health Sciences › Medicine › Genetics › Hemoglobinopathies and Related Disorders
- Keywords
- growth differentiation factor 15, GDF15, ineffective erythropoiesis, erythropoiesis, hepcidin, iron overload, thalassemia, congenital dyserythropoiesis, sideroblastic anemia, erythroblasts, apoptosis, bone marrow transplantation, TGF-beta superfamily
- MeSH terms
- Anemia, Animals, Erythropoiesis, Humans, Thalassemia, Iron Overload, Growth Differentiation Factor 15
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