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 (646 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
Progenitor cells from which all blood cells derived. They are found primarily in the bone marrow and also in small numbers in the peripheral blood.
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: Cell, Hematopoietic Stem; Cells, Hematopoietic Stem; Hematopoietic Stem Cell; Stem Cell, Hematopoietic; Stem Cells, Hematopoietic; Hematopoietic Progenitor Cells; Cell, Hematopoietic Progenitor; Cells, Hematopoietic Progenitor.
Where it fits in the MeSH classification
- Broader topics
- Bone Marrow Cells; Stem Cells
- Narrower topics
- Lymphoid Progenitor Cells; Myeloid Progenitor Cells; Hemangioblasts; Peripheral Blood Stem Cells
- See also
- Colony-Forming Units Assay
Research landscape
PubMed indexes 59,788 records tagged with the MeSH heading “Hematopoietic Stem Cells” (counts retrieved 2026-10-31). 7,240 of them (12.1%) were published from 2020 onward, and the busiest period so far is through 1999 with 23,761 records.
Reviews account for 8,115 records (13.6%) and meta-analyses for 34. Randomized controlled trials number 245 (0.4%) 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 | 23,761 |
| 2000-2009 | 13,604 |
| 2010-2019 | 15,183 |
| 2020 onward | 7,240 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 8,115 | 13.6% |
| Meta-analyses | 34 | 0.1% |
| Randomized controlled trials | 245 | 0.4% |
Method: PubMed query "Hematopoietic Stem Cells"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in anatomy and physiology
Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.
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 |
|---|---|---|---|---|
| Dynamics of microcompartment formation at the mitosis-to-G1 transition | 2025 | Research article Design not recorded in structured metadata | 27 | cc by PMID 41107486 · DOI · PMC12700819 |
| Targeting triple-negative breast cancer using cord-blood CD34⁺ HSPC-derived mesothelin-specific CAR-NKT cells with potent antitumor activity | 2025 | Research article Design not recorded in structured metadata | 26 | cc by PMID 41077583 · DOI · PMC12516852 |
| Clusterin drives myeloid bias in aged hematopoietic stem cells by regulating mitochondrial function | 2025 | Research article Design not recorded in structured metadata | 24 | cc by PMID 40588652 · DOI · PMC12350150 |
| 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 |
Dynamics of microcompartment formation at the mitosis-to-G1 transition [1]
Abstract reading summary — source excerpts
- Opening excerpt
- As cells exit mitosis and enter G1, chromosomes decompact and transcription is reestablished.
- Closing excerpt
- Our results suggest that compaction and homotypic affinity drive microcompartment formation, which may explain transient transcriptional spiking at mitotic exit.
- 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 (153 words)
As cells exit mitosis and enter G1, chromosomes decompact and transcription is reestablished. Hi-C studies have indicated that all interphase three-dimensional genome features, including A/B compartments, topologically associating domains and CCCTC-binding factor loops, are lost during mitosis. However, Hi-C is insensitive to features such as microcompartments, nested focal interactions between cis-regulatory elements. Here we apply region capture Micro-C to mouse erythroblasts from mitosis to G1. We unexpectedly observe microcompartments in prometaphase, which strengthen in anaphase and telophase before weakening throughout G1. Microcompartment anchors coincide with transcriptionally spiking promoters during mitosis. Loss of condensin loop extrusion differentially impacts microcompartments and A/B compartments, suggesting that they are partially distinct. Polymer modeling shows that microcompartment formation is favored by chromatin compaction and disfavored by loop extrusion, providing a basis for strong microcompartmentalization in anaphase and telophase. Our results suggest that compaction and homotypic affinity drive microcompartment formation, which may explain transient transcriptional spiking at mitotic exit.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41107486 · DOI · PMC12700819
Targeting triple-negative breast cancer using cord-blood CD34⁺ HSPC-derived mesothelin-specific CAR-NKT cells with potent antitumor activity [2]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundTriple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer characterized by the lack of ER, PR, and HER2 expression.
- Closing excerpt
- ConclusionsTogether, these results support Allo15MCAR-NKT cells as a next-generation, off-the-shelf immunotherapy with strong therapeutic potential for TNBC, particularly in the context of metastasis, immune evasion, and treatment resistance.
- 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 (196 words)
BackgroundTriple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer characterized by the lack of ER, PR, and HER2 expression. Its aggressive behavior, high degree of tumor heterogeneity, and immunosuppressive tumor microenvironment (TME) are associated with poor clinical outcomes, rapid disease progression, and limited therapeutic options. Although chimeric antigen receptor (CAR)-engineered T cell therapy has shown certain promise, its applicability in TNBC is hindered by antigen escape, TME-mediated suppression, and the logistical constraints of autologous cell production.MethodsIn this study, we employed hematopoietic stem and progenitor cell (HSPC) gene engineering and a feeder-free HSPC differentiation culture to generate allogeneic IL-15-enhanced, mesothelin-specific CAR-engineered invariant natural killer T (Allo15MCAR-NKT) cells.ResultsThese cells demonstrated robust and multifaceted antitumor activity against TNBC, mediated by CAR- and NK receptor-dependent cytotoxicity, as well as selective targeting of CD1d+ TME immunosuppressive cells through their TCR. In both orthotopic and metastatic TNBC xenograft models, Allo15MCAR-NKT cells demonstrated potent antitumor activity, associated with robust effector and cytotoxic phenotypes, low exhaustion, and a favorable safety profile without inducing graft-versus-host disease.ConclusionsTogether, these results support Allo15MCAR-NKT cells as a next-generation, off-the-shelf immunotherapy with strong therapeutic potential for TNBC, particularly in the context of metastasis, immune evasion, and treatment resistance.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41077583 · DOI · PMC12516852
Clusterin drives myeloid bias in aged hematopoietic stem cells by regulating mitochondrial function [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Aged hematopoietic stem cells (HSCs) exhibit diminished self-renewal and myeloid-biased differentiation with a decline in hematopoiesis and adaptive immune function.
- Closing excerpt
- Together, our data identify Clu as a critical regulator of aging-associated myeloid bias and reveal an Mfn2-OXPHOS-p38-Cebpb axis as the mechanism underlying how Clu upregulation in aged HSCs leads to myeloid-biased differentiation, providing a target for rejuvenation of aged hematopoietic and immune systems.
- 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 (146 words)
Aged hematopoietic stem cells (HSCs) exhibit diminished self-renewal and myeloid-biased differentiation with a decline in hematopoiesis and adaptive immune function. However, the molecular regulation of this impaired function remains largely unknown. Here, through an in vivo CRISPR-Cas9-based screen, we uncovered clusterin (Clu) as a driver of biased differentiation. Clu is upregulated in aged HSCs, and its knockout diminishes biased differentiation. Clu promotes mitochondrial hyperfusion by interacting with Mfn2 in aged HSCs, and its ablation attenuates oxidative phosphorylation, improves mitophagy, and reverses myeloid-biased differentiation via the OXPHOS-p38-Cebpb axis. Transplantation of Clu-depleted aged HSCs into middle-aged mice results in balanced hematopoiesis and improved physical functions. Together, our data identify Clu as a critical regulator of aging-associated myeloid bias and reveal an Mfn2-OXPHOS-p38-Cebpb axis as the mechanism underlying how Clu upregulation in aged HSCs leads to myeloid-biased differentiation, providing a target for rejuvenation of aged hematopoietic and immune systems.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40588652 · DOI · PMC12350150
Mutant p53 promotes clonal hematopoiesis by generating a chronic inflammatory microenvironment [4]
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
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 SARS-CoV-2 infection and overactivation of Nlrp3 inflammasome as a trigger of cytokine "storm" and risk factor for damage of hematopoietic stem cells [5]
- Research article Innate immune pathways and inflammation in hematopoietic aging, clonal hematopoiesis, and MDS [6]
- Research article Origins, Biology, and Diseases of Tissue Macrophages [7]
- Research article Hematopoietic stem cells through the ages: A lifetime of adaptation to organismal demands [8]
- Research article Erythroferrone structure, function, and physiology: Iron homeostasis and beyond [9]
- Research article Inflammatory signaling regulates hematopoietic stem and progenitor cell development and homeostasis [10]
References
- Goel VY, Aboreden NG, Jusuf JM, Zhang H, Mori LP, Mirny LA, et al.. Dynamics of microcompartment formation at the mitosis-to-G1 transition. . 2025. PMID 41107486 · DOI · PMC12700819
- Li YR, Shen X, Zhu Y, Li Z, Hon R, Tian Y, et al.. Targeting triple-negative breast cancer using cord-blood CD34⁺ HSPC-derived mesothelin-specific CAR-NKT cells with potent antitumor activity. . 2025. PMID 41077583 · DOI · PMC12516852
- Sun N, Lin CH, Li MY, Wang Y, Chen D, Ren X, et al.. Clusterin drives myeloid bias in aged hematopoietic stem cells by regulating mitochondrial function. . 2025. PMID 40588652 · DOI · PMC12350150
- 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
- Ratajczak MZ, Kucia M. SARS-CoV-2 infection and overactivation of Nlrp3 inflammasome as a trigger of cytokine "storm" and risk factor for damage of hematopoietic stem cells. Leukemia. 2020. PMID 32483300 · DOI · PMC7262681
- Trowbridge JJ, Starczynowski DT. Innate immune pathways and inflammation in hematopoietic aging, clonal hematopoiesis, and MDS. J Exp Med. 2021. PMID 34129017 · DOI · PMC8210621
- Cox N, Pokrovskii M, Vicario R, Geissmann F. Origins, Biology, and Diseases of Tissue Macrophages. Annu Rev Immunol. 2021. PMID 33902313 · DOI · PMC10786183
- Kasbekar M, Mitchell CA, Proven MA, Passegué E. Hematopoietic stem cells through the ages: A lifetime of adaptation to organismal demands. Cell Stem Cell. 2023. PMID 37865087 · DOI · PMC10842631
- Srole DN, Ganz T. Erythroferrone structure, function, and physiology: Iron homeostasis and beyond. J Cell Physiol. 2021. PMID 33372284 · DOI · PMC8026552
- Collins A, Mitchell CA, Passegué E. Inflammatory signaling regulates hematopoietic stem and progenitor cell development and homeostasis. J Exp Med. 2021. PMID 34129018 · DOI · PMC8210624
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 2026-10-31.
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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.