ArticleBlood advances2020
The transition of M-CSF-derived human macrophages to a growth-promoting phenotype.
Article in Blood advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 32 citations in OpenAlex.
- Sex-specific skeletal muscle fiber atrophy and reduced macrophage inflammation in a rodent transverse aortic constriction model.Pflugers Archiv : European journal of physiology · 2026Article
- A nucleic acid labeling chemistry reveals surface DNA on exosomes.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- SHIP blocks (MDP + LPS)-induced synergy in macrophages independent of catalytic activity.Journal of leukocyte biology · 2026Article
- Comprehensive Lipidomic Profiling Reveals Distinct Metabolic Remodeling during Differentiation of Human Monocyte-Derived Macrophages.Journal of proteome research · 2026Article
- M-CSF priming enhances the efficiency and reproducibility of hiPSC-derived osteoclast differentiation and pharmacological responsiveness to anti-resorptive agents.Scientific reports · 2026Article
- Recognition of Brucella abortus drives M2 like polarization and impaired antigen presentation in monocyte derived macrophages.Scientific reports · 2026Article
- Neuro-immune-bone axis in post-traumatic bone regeneration: temporal regulation, dysregulation mechanisms, and therapeutic implications.Frontiers in immunology · 2026Review
- Host-pathogen-immune interactions in an air-liquid interface airway model.Frontiers in cellular and infection microbiology · 2026Article
- CD300e is a driver of the immunosuppressive tumor microenvironment and colorectal cancer progression via macrophage reprogramming.Journal for immunotherapy of cancer · 2025Article
- Plasma Fibronectin Drives Macrophage Elongation via Integrin β3-Tie2 Axis in Blood Clots.Cancers · 2025Article
- Cannabinoid Receptor 2 (CB2) in Macrophages: A Promising Clinical Target for Immune Disorders.International journal of molecular sciences · 2025Review
- Review
- Promotion Mechanisms of Stromal Cell-Mediated Lung Cancer Development Within Tumor Microenvironment.Cancer management and research · 2025Review
- Mechanisms of prostatic inflammation-mediated male lower urinary tract symptoms.American journal of clinical and experimental urology · 2025Review
- Article
- Mendelian randomization reveals interactions of the blood proteome and immunome in mitral valve prolapse.Communications medicine · 2024Article
- Article
- Radical-Generating Activity, Phagocytosis, and Mechanical Properties of Four Phenotypes of Human Macrophages.International journal of molecular sciences · 2024Article
- Cellular and microenvironmental cues that promote macrophage fusion and foreign body response.Frontiers in immunology · 2024Article
- Macrophage variants in laboratory research: most are well done, but some are RAW.Frontiers in cellular and infection microbiology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Stimulated macrophages are potent producers of inflammatory mediators. This activity is highly regulated, in part, by resolving molecules to prevent tissue damage. In this study, we demonstrate that inflammation induced by Toll-like receptor stimulation is followed by the upregulation of receptors for adenosine (Ado) and prostaglandin E2 (PGE2), which help terminate macrophage activation and initiate tissue remodeling and angiogenesis. Macrophages can be hematopoietically derived from monocytes in response to 2 growth factors: macrophage colony-stimulating factor (M-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF). We examine how exposure to either of these differentiation factors shapes the macrophage response to resolving molecules. We analyzed the transcriptomes of human monocyte-derived macrophages stimulated in the presence of Ado or PGE2 and demonstrated that, in macrophages differentiated in M-CSF, Ado and PGE2 induce a shared transcriptional program involving the downregulation of inflammatory mediators and the upregulation of growth factors. In contrast, macrophages generated in GM-CSF fail to convert to a growth-promoting phenotype, which we attribute to the suppression of receptors for Ado and PGE2 and lower production of these endogenous regulators. These observations indicate that M-CSF macrophages are better prepared to transition to a program of tissue repair, whereas GM-CSF macrophages undergo more profound activation. We implicate the differential sensitivity to pro-resolving mediators as a contributor to these divergent phenotypes. This research highlights a number of molecular targets that can be exploited to regulate the strength and duration of macrophage activation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.