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 (646 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 relatively long-lived phagocytic cell of mammalian tissues that are derived from blood monocytes. Main types are peritoneal macrophages; alveolar macrophages; histiocytes; kupffer cells of the liver; and osteoclasts. They may further differentiate within chronic inflammatory lesions to epithelioid cells or may fuse to form foreign body giant cells or langhans giant cells. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.)
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: Monocyte-Derived Macrophages; Monocyte Derived Macrophages; Macrophage; Macrophages, Monocyte-Derived; Macrophage, Monocyte-Derived; Macrophages, Monocyte Derived; Monocyte-Derived Macrophage; Bone Marrow-Derived Macrophages.
Where it fits in the MeSH classification
- Broader topics
- Connective Tissue Cells; Myeloid Cells; Phagocytes; Mononuclear Phagocyte System
- Narrower topics
- Epithelioid Cells; Foam Cells; Giant Cells, Foreign-Body; Giant Cells, Langhans; Histiocytes; Kupffer Cells; Macrophages, Alveolar; Macrophages, Peritoneal; Osteoclasts; Tumor-Associated Macrophages; Monocyte-Macrophage Precursor Cells; RAW 264.7 Cells
- See also
- Phagocytosis
Related concepts
- Monocytes
- Peritoneal Macrophages
- Alveolar Macrophages
- Histiocytes
- Kupffer Cells
- Osteoclasts
- Epithelioid Cells
- Foreign Body Giant Cells
- Langhans Giant Cells
Research landscape
PubMed indexes 243,201 records tagged with the MeSH heading “Macrophages” (counts retrieved 2026-10-31). 59,565 of them (24.5%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 70,052 records.
Reviews account for 21,750 records (8.9%) and meta-analyses for 88. Randomized controlled trials number 484 (0.2%) 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 | 68,839 |
| 2000-2009 | 44,745 |
| 2010-2019 | 70,052 |
| 2020 onward | 59,565 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 21,750 | 8.9% |
| Meta-analyses | 88 | 0.0% |
| Randomized controlled trials | 484 | 0.2% |
Method: PubMed query "Macrophages"[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 |
|---|---|---|---|---|
| Tubular epithelial cells promote macrophage pyroptosis through PANX1-extracellular ATP-P2X7 signaling in aldosterone-dependent renal injury | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42552307 · DOI · PMC13438567 |
| 2-Deoxyglucose Dendrimer-Enabled Niclosamide Delivery to FRβ-Expressing Macrophages Alleviates Endometriosis Progression and Associated Hyperalgesia | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42670248 · DOI · PMC13650810 |
| Suidae iPSC-derived macrophages as models for investigating susceptibility and resilience to African swine fever virus | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42561938 · DOI · PMC13555459 |
Tubular epithelial cells promote macrophage pyroptosis through PANX1-extracellular ATP-P2X7 signaling in aldosterone-dependent renal injury [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Tubular epithelial cell (TEC)-macrophage crosstalk contributes to aldosterone (Aldo)-dependent renal fibrosis in hypertension.
- Closing excerpt
- Mechanism through which Aldo/MR-induced PANX1-eATP-P2X7 signaling activation promotes macrophage pyroptosis in hypertensive renal injury.
- 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 (301 words)
Tubular epithelial cell (TEC)-macrophage crosstalk contributes to aldosterone (Aldo)-dependent renal fibrosis in hypertension. Extracellular ATP (eATP) can act as a mediator of TEC-macrophage crosstalk. However, whether and how eATP functions in Aldo-induced renal injury remain unknown. A deoxycorticosterone acetate (DOCA)-salt-induced hypertensive mouse model and a primary mouse renal tubular epithelial cell (mTEC)-bone marrow-derived macrophage (BMDM) coculture model were developed. To investigate the relationship between Aldo/MR and eATP signaling in TEC-macrophage crosstalk, specific inhibitors, adeno-associated virus (AAV)-shRNA and small interfering RNA (siRNA) were used. scRNA-seq analysis of kidneys from DOCA-salt mice was performed for verification. Urinary ATP levels and renal pannexin1 (PANX1, an ATP efflux channel) expression increased significantly in DOCA-salt mice, whereas the selective mineralocorticoid receptor (MR) antagonist finerenone treatment reduced urinary ATP levels, PANX1 expression, tubular injury, and macrophage-related inflammation. Inhibiting PANX1-eATP-P2X7 signaling with the PANX1 inhibitor probenecid, specifically knocking down tubular PANX1, or using the eATP ectonucleotidase apyrase or the P2X7 blocker AZ10606120 mitigated renal tubular damage and NLRP3-mediated pyroptosis in the renal cortex of DOCA-salt mice. Similarly, in mTECs, finerenone suppressed Aldo-induced ATP release and PANX1 upregulation. A luciferase assay confirmed the binding site of MR to the PANX1 transcription promoter. Coculture of BMDMs with mTECs under Aldo stimulation significantly increased NLRP3-mediated BMDM pyroptosis and migration. However, these effects were reversed by treating the mTECs with MR or PANX1 siRNA. Similar results were observed after treatment with apyrase or AZ10606120 in the coculture system. scRNA-seq analysis further identified the activation of P2X7/NLRP3-related pyroptosis pathway in macrophages from DOCA-salt mice. In conclusion, TECs play a critical role in macrophage pyroptosis in Aldo-induced renal injury. eATP is a key messenger involved in TEC-macrophage crosstalk. PANX1-eATP-P2X7 signaling mediates TEC‒macrophage interactions to exacerbate Aldo-driven renal inflammation in hypertension. Mechanism through which Aldo/MR-induced PANX1-eATP-P2X7 signaling activation promotes macrophage pyroptosis in hypertensive renal injury.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42552307 · DOI · PMC13438567
2-Deoxyglucose Dendrimer-Enabled Niclosamide Delivery to FRβ-Expressing Macrophages Alleviates Endometriosis Progression and Associated Hyperalgesia [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Endometriosis (EuE) is a chronic, incurable disease.
- Closing excerpt
- Together, these findings establish FRβ+ macrophages as a potential target in EuE and present FA-2DG-D-Niclo as a nonhormonal, macrophage-focused nanomedicine for precise and effective endometriosis treatment.
- 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 (195 words)
Endometriosis (EuE) is a chronic, incurable disease. Due to limited efficacy, high recurrence rates, and serious side effects of current treatments, development of new, targeted, nonhormonal therapies is urgently needed. We previously reported that niclosamide, an FDA-approved anthelmintic drug, attenuates endometriotic lesion growth. We further identified folate receptor-β (FRβ)-positive macrophages as contributors to disease progression. Significantly, niclosamide inhibits FRβ+ macrophages and reduces inflammation, innervation, and angiogenesis. To develop niclosamide as a nonhormonal and selective immune cell-targeted therapy for EuE, we engineered a folic acid (FA)-conjugated 2-deoxyglucose dendrimer (FA-2DG-D) using click chemistry to enable selective FRβ-mediated uptake. Conjugation of niclosamide to FA-2DG-D yielded a targeted nanotherapeutic (FA-2DG-D-Niclo) with enhanced aqueous solubility, controlled intracellular release, and excellent batch-to-batch reproducibility. In a mouse model of EuE, FA-2DG-D demonstrated lesion-specific accumulation and selective internalization by FRβ+ macrophages with minimal off-target organ retention. A single intraperitoneal dose of FA-2DG-D-Niclo (25 or 50 mg/kg/bw of niclosamide) significantly reduced FRβ+ macrophage burden, suppressed lesion number and volume, and markedly improved EuE-associated hyperalgesia at 2 weeks post-treatment. Together, these findings establish FRβ+ macrophages as a potential target in EuE and present FA-2DG-D-Niclo as a nonhormonal, macrophage-focused nanomedicine for precise and effective endometriosis treatment.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42670248 · DOI · PMC13650810
Suidae iPSC-derived macrophages as models for investigating susceptibility and resilience to African swine fever virus [3]
Abstract reading summary — source excerpts
- Opening excerpt
- African swine fever virus (ASFV) causes a lethal hemorrhagic fever in pigs, and spread of this disease threatens many pig species (Suidae) globally.
- Closing excerpt
- iPSCdMs may therefore represent an experimental system to understand how ASFV infection of Mϕs contributes to disease and aid development of strategies to combat this economically and environmentally devastating pathogen.
- 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 (150 words)
African swine fever virus (ASFV) causes a lethal hemorrhagic fever in pigs, and spread of this disease threatens many pig species (Suidae) globally. By contrast, ASFV infections in the natural evolved hosts, warthog and bushpig, are subclinical. The macrophage (Mϕ) is the primary target of ASFV, and species-dependent responses in Mϕs are presumed to influence disease susceptibility. In an attempt to model these differences in vitro, we generated transgene-regulated induced pluripotent stem cells (iPSCs) from domestic pig, wild boar, red river hog, and warthog and confirmed that their corresponding iPSC-derived Mϕs (iPSCdMs) supported infection and replication of ASFV. In contrast to the other species, however, warthog iPSCdMs did not induce interferon α upon infection by either virulent or attenuated ASFV. iPSCdMs may therefore represent an experimental system to understand how ASFV infection of Mϕs contributes to disease and aid development of strategies to combat this economically and environmentally devastating pathogen.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42561938 · DOI · PMC13555459
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 Prognostic significance of tumor-associated macrophages in solid tumor: a meta-analysis of the literature [4]
- Research article Prognostic significance of tumor-associated macrophages in breast cancer: a meta-analysis of the literature [5]
- Research article Prognostic significance of tumor-associated macrophages in ovarian cancer: A meta-analysis [6]
- Research article Prognostic impact of tumor-associated macrophage infiltration in non-small cell lung cancer: A systemic review and meta-analysis [7]
- Research article Inflammatory biomarkers on an LPS-induced RAW 264.7 cell model: a systematic review and meta-analysis [8]
- Research article Comprehensive gene expression meta-analysis identifies signature genes that distinguish microglia from peripheral monocytes/macrophages in health and glioma [9]
References
- Wang C, Ma H, Xu J, Tang Y, Feng J, Yang Y, et al.. Tubular epithelial cells promote macrophage pyroptosis through PANX1-extracellular ATP-P2X7 signaling in aldosterone-dependent renal injury. . 2026. PMID 42552307 · DOI · PMC13438567
- Dhull A, Shi M, Harvey ME, Page TM, Sharma R, Goody KJ, et al.. 2-Deoxyglucose Dendrimer-Enabled Niclosamide Delivery to FRβ-Expressing Macrophages Alleviates Endometriosis Progression and Associated Hyperalgesia. . 2026. PMID 42670248 · DOI · PMC13650810
- Watson TM, Goatley LC, Meek S, Eory L, Kohler S, Berkley N, et al.. Suidae iPSC-derived macrophages as models for investigating susceptibility and resilience to African swine fever virus. . 2026. PMID 42561938 · DOI · PMC13555459
- Zhang QW, Liu L, Gong CY, Shi HS, Zeng YH, Wang XZ, et al.. Prognostic significance of tumor-associated macrophages in solid tumor: a meta-analysis of the literature. PLoS One. 2012. PMID 23284651 · DOI · PMC3532403
- Zhao X, Qu J, Sun Y, Wang J, Liu X, Wang F, et al.. Prognostic significance of tumor-associated macrophages in breast cancer: a meta-analysis of the literature. Oncotarget. 2017. PMID 28427165 · DOI · PMC5444766
- Yuan X, Zhang J, Li D, Mao Y, Mo F, Du W, et al.. Prognostic significance of tumor-associated macrophages in ovarian cancer: A meta-analysis. Gynecol Oncol. 2017. PMID 28698008 · DOI
- Mei J, Xiao Z, Guo C, Pu Q, Ma L, Liu C, et al.. Prognostic impact of tumor-associated macrophage infiltration in non-small cell lung cancer: A systemic review and meta-analysis. Oncotarget. 2016. PMID 27144518 · DOI · PMC5085150
- Facchin BM, Dos Reis GO, Vieira GN, Mohr ETB, da Rosa JS, Kretzer IF, et al.. Inflammatory biomarkers on an LPS-induced RAW 264.7 cell model: a systematic review and meta-analysis. Inflamm Res. 2022. PMID 35612604 · DOI
- Haage V, Semtner M, Vidal RO, Hernandez DP, Pong WW, Chen Z, et al.. Comprehensive gene expression meta-analysis identifies signature genes that distinguish microglia from peripheral monocytes/macrophages in health and glioma. Acta Neuropathol Commun. 2019. PMID 30764877 · DOI · PMC6376799
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.