Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (645 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
The production of red blood cells (erythrocytes). In humans, erythrocytes are produced by the yolk sac in the first trimester; by the liver in the second trimester; by the bone marrow in the third trimester and after birth. In normal individuals, the erythrocyte count in the peripheral blood remains relatively constant implying a balance between the rate of erythrocyte production and rate of destruction.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Erythropoieses.
Where it fits in the MeSH classification
- Broader topics
- Hematopoiesis
Related concepts
Research landscape
PubMed indexes 14,617 records tagged with the MeSH heading “Erythropoiesis” (counts retrieved 2026-10-29). 1,214 of them (8.3%) were published from 2020 onward, and the busiest period so far is through 1999 with 9,383 records.
Reviews account for 1,893 records (13.0%) and meta-analyses for 28. Randomized controlled trials number 215 (1.5%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 9,383 |
| 2000-2009 | 1,899 |
| 2010-2019 | 2,121 |
| 2020 onward | 1,214 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 1,893 | 13.0% |
| Meta-analyses | 28 | 0.2% |
| Randomized controlled trials | 215 | 1.5% |
Method: PubMed query "Erythropoiesis"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in molecular biology
Molecular biology establishes mechanisms through controlled experiments, often in simplified systems such as purified proteins, cultured cells or model organisms. Such work can show what is possible in a defined system, but whether a pathway matters in a whole organism or in human disease needs further evidence. Check the experimental system, whether findings were reproduced by independent groups, and whether the authors tested the mechanism directly or inferred it from correlation.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Stress Erythropoiesis is a Key Inflammatory Response | 2020 | Review article Design not recorded in structured metadata | 91 | cc by PMID 32155728 · DOI · PMC7140438 |
| The Role of PI3K/AKT and MAPK Signaling Pathways in Erythropoietin Signalization | 2021 | Review article Design not recorded in structured metadata | 90 | cc by PMID 34299300 · DOI · PMC8307237 |
| Canagliflozin Improves Erythropoiesis in Diabetes Patients with Anemia of Chronic Kidney Disease | 2019 | Research article Design not recorded in structured metadata | 78 | cc by PMID 31385724 · DOI · PMC6875696 |
| Loop extrusion by cohesin plays a role in enhancer-activated gene expression early in differentiation | 2026 | Research article Design not recorded in structured metadata | 10 | cc by PMID 42192110 · DOI · PMC13402345 |
Stress Erythropoiesis is a Key Inflammatory Response [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Bone marrow medullary erythropoiesis is primarily homeostatic.
- Closing excerpt
- We propose a new hypothesis that stress erythropoiesis is induced by inflammation and plays a key role in maintaining erythroid homeostasis during inflammatory responses.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (125 words)
Bone marrow medullary erythropoiesis is primarily homeostatic. It produces new erythrocytes at a constant rate, which is balanced by the turnover of senescent erythrocytes by macrophages in the spleen. Despite the enormous capacity of the bone marrow to produce erythrocytes, there are times when it is unable to keep pace with erythroid demand. At these times stress erythropoiesis predominates. Stress erythropoiesis generates a large bolus of new erythrocytes to maintain homeostasis until steady state erythropoiesis can resume. In this review, we outline the mechanistic differences between stress erythropoiesis and steady state erythropoiesis and show that their responses to inflammation are complementary. We propose a new hypothesis that stress erythropoiesis is induced by inflammation and plays a key role in maintaining erythroid homeostasis during inflammatory responses.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32155728 · DOI · PMC7140438
The Role of PI3K/AKT and MAPK Signaling Pathways in Erythropoietin Signalization [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Erythropoietin (EPO) is a glycoprotein cytokine known for its pleiotropic effects on various types of cells and tissues.
- Closing excerpt
- We summarize the current state of research in this field, highlight the novel members of EPO-induced PI3K and MAPK signaling, and in this respect also the differences between erythroid and non-erythroid cells.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (120 words)
Erythropoietin (EPO) is a glycoprotein cytokine known for its pleiotropic effects on various types of cells and tissues. EPO and its receptor EPOR trigger signaling cascades JAK2/STAT5, MAPK, and PI3K/AKT that are interconnected and irreplaceable for cell survival. In this article, we describe the role of the MAPK and PI3K/AKT signaling pathways during red blood cell formation as well as in non-hematopoietic tissues and tumor cells. Although the central framework of these pathways is similar for most of cell types, there are some stage-specific, tissue, and cell-lineage differences. We summarize the current state of research in this field, highlight the novel members of EPO-induced PI3K and MAPK signaling, and in this respect also the differences between erythroid and non-erythroid cells.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34299300 · DOI · PMC8307237
Canagliflozin Improves Erythropoiesis in Diabetes Patients with Anemia of Chronic Kidney Disease [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Background: We evaluated the erythropoietic effects of canagliflozin, a sodium-glucose cotransporter 2 inhibitor, in type 2 diabetes patients with anemia of chronic kidney disease.
- Closing excerpt
- The effect on erythropoiesis appeared to be due to an EPO production-mediated mechanism and might be independent of glycemic control; however, further studies are needed to clarify this since the present study had a small sample size and no comparator group.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (252 words)
Background: We evaluated the erythropoietic effects of canagliflozin, a sodium-glucose cotransporter 2 inhibitor, in type 2 diabetes patients with anemia of chronic kidney disease. Methods: Nine diabetes patients were enrolled and administered 100 mg canagliflozin once a day for 12 weeks. The patients received fixed doses of conventional antidiabetic drugs and renin-angiotensin system inhibitors for 8 weeks before enrollment; these drugs were continued during the study. Endpoints were changes in erythropoiesis parameters, including erythrocyte and reticulocyte count, hemoglobin, hematocrit, and serum erythropoietin (EPO) concentration from baseline to 12 weeks. All variables were measured every 2 weeks. Results: Serum EPO concentration increased by 38 [15-62]% (P = 0.043) between baseline and 2 and 4 weeks. Reticulocyte count transiently increased at 2 weeks. Erythropoiesis occurred after 2 weeks of canagliflozin treatment. Erythrocyte count (from 386 ± 36 × 104/μL to 421 ± 36 × 104/μL; P = 0.0009), hemoglobin (from 11.8 ± 0.6 g/dL to 12.9 ± 1.1 g/dL; P = 0.0049), and hematocrit (from 37.1 ± 2.3% to 40.4 ± 3.2%; P = 0.002) increased from baseline to study completion. Although there were no significant changes in transferrin saturation, serum ferritin levels were decreased (P = 0.003). Conclusions: Canagliflozin treatment led to an improvement in erythropoiesis in patients with impaired kidney function. The effect on erythropoiesis appeared to be due to an EPO production-mediated mechanism and might be independent of glycemic control; however, further studies are needed to clarify this since the present study had a small sample size and no comparator group.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31385724 · DOI · PMC6875696
Loop extrusion by cohesin plays a role in enhancer-activated gene expression early in differentiation [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Enhancers and their target promoters often come into close physical proximity when activated.
- Closing excerpt
- We find that loop extrusion does play an important role in establishing enhancer-promoter proximity and consequent expression of inducible genes during differentiation.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (148 words)
Enhancers and their target promoters often come into close physical proximity when activated. This may be explained by a variety of mechanisms, including cohesin-mediated chromatin loop extrusion. However, acute depletion of cohesin does not cause widespread changes in gene expression. We have tested the role of cohesin-mediated loop extrusion in gene expression at the mouse alpha-globin locus during erythropoiesis. Acute depletion of cohesin disrupts alpha-globin expression at early but not late stages of differentiation. Furthermore, when single or multiple CTCF sites, known to block cohesin, are placed between the alpha-globin enhancers and promoters, alpha-gene expression is disrupted. Importantly, the CTCF site's orientation is critical, suggesting that within this activated domain, in definitive erythroid cells, cohesin predominantly but not exclusively, translocates from the enhancers to the promoters. We find that loop extrusion does play an important role in establishing enhancer-promoter proximity and consequent expression of inducible genes during differentiation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42192110 · DOI · PMC13402345
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Regulation of erythropoiesis by hypoxia-inducible factors [5]
- Research article Ironing out Ferroportin [6]
- Research article PI3K/Akt signaling transduction pathway, erythropoiesis and glycolysis in hypoxia (Review) [7]
- Research article Regulation of erythropoietin production [8]
- Research article New insights into erythropoiesis: the roles of folate, vitamin B12, and iron [9]
- Research article Erythropoiesis: development and differentiation [10]
References
- Paulson RF, Ruan B, Hao S, Chen Y. Stress Erythropoiesis is a Key Inflammatory Response. . 2020. PMID 32155728 · DOI · PMC7140438
- Tóthová Z, Šemeláková M, Solárová Z, Tomc J, Debeljak N, Solár P. The Role of PI3K/AKT and MAPK Signaling Pathways in Erythropoietin Signalization. . 2021. PMID 34299300 · DOI · PMC8307237
- Maruyama T, Takashima H, Oguma H, Nakamura Y, Ohno M, Utsunomiya K, et al.. Canagliflozin Improves Erythropoiesis in Diabetes Patients with Anemia of Chronic Kidney Disease. . 2019. PMID 31385724 · DOI · PMC6875696
- Stolper RJ, Tsang FH, Georgiades E, Hanssen LLP, Tunnacliffe EAJ, Downes DJ, et al.. Loop extrusion by cohesin plays a role in enhancer-activated gene expression early in differentiation. . 2026. PMID 42192110 · DOI · PMC13402345
- Haase VH. Regulation of erythropoiesis by hypoxia-inducible factors. Blood Rev. 2013. PMID 23291219 · DOI · PMC3731139
- Drakesmith H, Nemeth E, Ganz T. Ironing out Ferroportin. Cell Metab. 2015. PMID 26437604 · DOI · PMC4635047
- Xie Y, Shi X, Sheng K, Han G, Li W, Zhao Q, et al.. PI3K/Akt signaling transduction pathway, erythropoiesis and glycolysis in hypoxia (Review). Mol Med Rep. 2019. PMID 30535469 · DOI · PMC6323245
- Jelkmann W. Regulation of erythropoietin production. J Physiol. 2011. PMID 21078592 · DOI
- Koury MJ, Ponka P. New insights into erythropoiesis: the roles of folate, vitamin B12, and iron. Annu Rev Nutr. 2004. PMID 15189115 · DOI
- Dzierzak E, Philipsen S. Erythropoiesis: development and differentiation. Cold Spring Harb Perspect Med. 2013. PMID 23545573 · DOI · PMC3684002
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.