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: 3 complete abstracts (518 words), 9 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 development and formation of various types of blood cells. Hematopoiesis can take place in the bone marrow (medullary) or outside the bone marrow (hematopoiesis, extramedullary).
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: Haematopoiesis; Hematopoiesis, Medullary; Medullary Hematopoiesis.
Where it fits in the MeSH classification
- Broader topics
- Cell Differentiation; Blood Physiological Phenomena
- Narrower topics
- Clonal Hematopoiesis; Erythropoiesis; Hematopoiesis, Extramedullary; Leukopoiesis; Thrombopoiesis
Related concepts
- Blood Cells
- Bone Marrow
- Hematopoiesis
- Extramedullary
Research landscape
PubMed indexes 46,338 records tagged with the MeSH heading “Hematopoiesis” (counts retrieved 2026-10-29). 5,815 of them (12.5%) were published from 2020 onward, and the busiest period so far is through 1999 with 23,285 records.
Reviews account for 8,284 records (17.9%) and meta-analyses for 59. Randomized controlled trials number 372 (0.8%) 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 | 23,285 |
| 2000-2009 | 8,034 |
| 2010-2019 | 9,204 |
| 2020 onward | 5,815 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 8,284 | 17.9% |
| Meta-analyses | 59 | 0.1% |
| Randomized controlled trials | 372 | 0.8% |
Method: PubMed query "Hematopoiesis"[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 |
|---|---|---|---|---|
| Inflammatory stromal and T cells mediate human bone marrow niche remodeling in clonal hematopoiesis and myelodysplasia | 2025 | Research article Design not recorded in structured metadata | 21 | cc by PMID 41253811 · DOI · PMC12627676 |
| Mutant p53 promotes clonal hematopoiesis by generating a chronic inflammatory microenvironment | 2026 | Research article Design not recorded in structured metadata | 13 | cc by PMID 41468163 · DOI · PMC12867160 |
| ASXL1 mutation-related clonal hematopoiesis and age-related diseases: clinical evidence and molecular insights | 2025 | Review article Design not recorded in structured metadata | 12 | cc by PMID 40773119 · DOI · PMC12380941 |
Inflammatory stromal and T cells mediate human bone marrow niche remodeling in clonal hematopoiesis and myelodysplasia [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Somatic mutations in hematopoietic stem/progenitor cells (HSPCs) can lead to clonal hematopoiesis of indeterminate potential (CHIP) and progression to myelodysplastic syndromes (MDS).
- Closing excerpt
- These findings position iMSCs as central mediators of early BM niche dysfunction and potential therapeutic targets for intercepting pre-malignant hematopoiesis.
- 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 (175 words)
Somatic mutations in hematopoietic stem/progenitor cells (HSPCs) can lead to clonal hematopoiesis of indeterminate potential (CHIP) and progression to myelodysplastic syndromes (MDS). Using single-cell and anatomical profiling of a large cohort of human bone marrow (BM), we show that the HSPC BM niche in CHIP and MDS is undergoing inflammatory remodeling. This includes loss of CXCL12⁺ adipogenic stromal cells and the emergence of a distinct population of inflammatory mesenchymal stromal cells (iMSCs), which arise in CHIP and become more prevalent in MDS. Functional studies in primary BM HSPC-MSC co-cultures reveals that healthy aged and CHIP HSPCs activate stromal support, while MDS HSPCs fail to do so. In contrast, MDS blasts further suppress HSPC support and trigger inflammation, indicating disease-stage-specific stromal disruption. In parallel, we show that iMSCs retain partial support and angiogenic potential in MDS, coinciding with expanded BM vasculature. Additionally, we identify IFN-responsive T cells that preferentially interact with iMSCs, potentially reinforcing local inflammation. These findings position iMSCs as central mediators of early BM niche dysfunction and potential therapeutic targets for intercepting pre-malignant hematopoiesis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41253811 · DOI · PMC12627676
Mutant p53 promotes clonal hematopoiesis by generating a chronic inflammatory microenvironment [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Older individuals with somatic TP53 mutations manifest clonal hematopoiesis (CH) and are at high risk of developing myeloid neoplasms.
- Closing excerpt
- Thus, our findings uncover an important role for mutant p53 in regulating inflammatory signaling in CH and suggest that curbing inflammation may prevent the progression of TP53-mutant CH to myeloid neoplasms.
- 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 (151 words)
Older individuals with somatic TP53 mutations manifest clonal hematopoiesis (CH) and are at high risk of developing myeloid neoplasms. However, the underlying mechanisms are not fully understood. Here, we show that inflammatory stress confers a competitive advantage to p53 mutant hematopoietic stem and progenitor cells (HSPCs) by activating the NLRP1 inflammasome and increasing the secretion of pro-inflammatory cytokines such as IL-1β, inhibiting WT HSPC fitness in a paracrine fashion. During aging, mutant p53 dysregulates pre-mRNA splicing in HSPCs, leading to enhanced NF-κB activation and increased secretion of IL-1β and IL-6, thereby generating a chronic inflammatory bone marrow microenvironment. Furthermore, blocking IL-1β with IL-1β neutralizing antibody or inhibiting IL-1β secretion using gasdermin D inhibitor decreases the fitness of p53 mutant HSPCs. Thus, our findings uncover an important role for mutant p53 in regulating inflammatory signaling in CH and suggest that curbing inflammation may prevent the progression of TP53-mutant CH to myeloid neoplasms.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41468163 · DOI · PMC12867160
ASXL1 mutation-related clonal hematopoiesis and age-related diseases: clinical evidence and molecular insights [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Clonal hematopoiesis (CH) is defined as the age-associated expansion of hematopoietic stem and progenitor cells harboring somatic mutations, most frequently in epigenetic regulators such as DNMT3A, TET2, and ASXL1.
- Closing excerpt
- By integrating clinical observations and emerging mechanistic data, we highlight the urgent need for deeper investigation into ASXL1-driven CH and its systemic consequences beyond hematological transformation.
- 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 (192 words)
Clonal hematopoiesis (CH) is defined as the age-associated expansion of hematopoietic stem and progenitor cells harboring somatic mutations, most frequently in epigenetic regulators such as DNMT3A, TET2, and ASXL1. Although CH was initially recognized as a precursor to hematological malignancies, accumulating evidence has led to its broad recognition as a relevant factor in various age-related nonmalignant diseases, particularly those with inflammatory components, such as cardiovascular disease, autoimmune disorders, and solid tumors. Notably, the increased overall mortality associated with CH is primarily driven by cardiovascular complications rather than hematological malignancies. Among CH-associated genes, ASXL1 mutations are distinguished by their strong associations with adverse clinical outcomes and pro-inflammatory signatures. However, compared to TET2 and DNMT3A, the molecular and pathological implications of ASXL1-mutated CH remain underexplored. Recent studies have expanded the disease spectrum of ASXL1 mutations beyond hematological malignancies, implicating them in clonal expansion and systemic inflammation. This review aims to summarize the current epidemiological and experimental insights into ASXL1-mutated CH, focusing on its potential contributions to inflammation-associated diseases. By integrating clinical observations and emerging mechanistic data, we highlight the urgent need for deeper investigation into ASXL1-driven CH and its systemic consequences beyond hematological transformation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40773119 · DOI · PMC12380941
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 Niches that regulate stem cells and hematopoiesis in adult bone marrow [4]
- Research article The CD70-CD27 axis in oncology: the new kids on the block [5]
- Research article Clonal hematopoiesis: Mutation-specific adaptation to environmental change [6]
- Research article Made to order: emergency myelopoiesis and demand-adapted innate immune cell production [7]
- Research article Clonal hematopoiesis, somatic mosaicism, and age-associated disease [8]
- Research article Inflammatory Modulation of Hematopoiesis: Linking Trained Immunity and Clonal Hematopoiesis with Chronic Disorders [9]
References
- Prummel KD, Woods K, Kholmatov M, Schmitt EC, Vlachou EP, Labyadh M, et al.. Inflammatory stromal and T cells mediate human bone marrow niche remodeling in clonal hematopoiesis and myelodysplasia. . 2025. PMID 41253811 · DOI · PMC12627676
- Chen S, Barajas S, Vemula S, Yang Y, Simpson E, Gao H, et al.. Mutant p53 promotes clonal hematopoiesis by generating a chronic inflammatory microenvironment. . 2026. PMID 41468163 · DOI · PMC12867160
- Sato N, Goyama S, Kitamura T. ASXL1 mutation-related clonal hematopoiesis and age-related diseases: clinical evidence and molecular insights. . 2025. PMID 40773119 · DOI · PMC12380941
- Comazzetto S, Shen B, Morrison SJ. Niches that regulate stem cells and hematopoiesis in adult bone marrow. Dev Cell. 2021. PMID 34146467 · DOI · PMC8282762
- Flieswasser T, Van den Eynde A, Van Audenaerde J, De Waele J, Lardon F, Riether C, et al.. The CD70-CD27 axis in oncology: the new kids on the block. J Exp Clin Cancer Res. 2022. PMID 34991665 · DOI · PMC8734249
- Florez MA, Tran BT, Wathan TK, DeGregori J, Pietras EM, King KY. Clonal hematopoiesis: Mutation-specific adaptation to environmental change. Cell Stem Cell. 2022. PMID 35659875 · DOI · PMC9202417
- Swann JW, Olson OC, Passegué E. Made to order: emergency myelopoiesis and demand-adapted innate immune cell production. Nat Rev Immunol. 2024. PMID 38467802 · DOI · PMC12942464
- Evans MA, Walsh K. Clonal hematopoiesis, somatic mosaicism, and age-associated disease. Physiol Rev. 2023. PMID 36049115 · DOI · PMC9639777
- Chavakis T, Wielockx B, Hajishengallis G. Inflammatory Modulation of Hematopoiesis: Linking Trained Immunity and Clonal Hematopoiesis with Chronic Disorders. Annu Rev Physiol. 2022. PMID 34614373 · DOI
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.