ArticleThe Journal of experimental medicine2021
PPARγ is essential for the development of bone marrow erythroblastic island macrophages and splenic red pulp macrophages.
Article in The Journal of experimental medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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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.
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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.
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Who cites it
27 citing papers in PubMed, 50 citations in OpenAlex.
- Canonical Notch2 signaling regulates development and maintenance of iron-recycling macrophages and iron homeostasis.Nature communications · 2026Article
- Multi-level transcriptional control of specific macrophage responses.The EMBO journal · 2026Review
- Ferroportin at the Crossroads of Iron Biology: Disease, Regulation and Modulation.Biomolecules · 2026Review
- Ferroptosis is a Physiologic Vulnerability of Iron-Recycling Macrophages.bioRxiv : the preprint server for biology · 2026Article
- Identity, ontogeny, and age-related changes in splenic white pulp macrophages in mouse and human spleen.bioRxiv : the preprint server for biology · 2026Article
- Review
- Article
- Loss of NR2F6 Protects from Salmonella Typhimurium Infection.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Single-Cell and Single-Nuclei transcriptomics profiling reveals dynamic cellular features in tumor-related adipose microenvironment of breast cancer patients with high BMI.Translational oncology · 2025Article
- Tissue macrophages: origin, heterogenity, biological functions, diseases and therapeutic targets.Signal transduction and targeted therapy · 2025Review
- Lipid synthesis, triggered by PPARγ T166 dephosphorylation, sustains reparative function of macrophages during tissue repair.Nature communications · 2024Article
- TFPI from erythroblasts drives heme production in central macrophages promoting erythropoiesis in polycythemia.Nature communications · 2024Article
- CD169-CD43 interaction is involved in erythroblastic island formation and erythroid differentiation.Haematologica · 2023Article
- Circulating miRNAs Expression in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.International journal of molecular sciences · 2023Article
- Article
- Genipin-activating PPARγ impedes CCR2-mediated macrophage infiltration into postoperative liver to suppress recurrence of hepatocellular carcinoma.International journal of biological sciences · 2023Article
- Establishment of tissue-resident immune populations in the fetus.Seminars in immunopathology · 2022Review
- RXRα Regulates the Development of Resident Tissue Macrophages.ImmunoHorizons · 2022Article
- EP3 enhances adhesion and cytotoxicity of NK cells toward hepatic stellate cells in a murine liver fibrosis model.The Journal of experimental medicine · 2022Article
- The impact of the lung environment on macrophage development, activation and function: diversity in the face of adversity.Mucosal immunology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tissue-resident macrophages play a crucial role in maintaining homeostasis. Macrophage progenitors migrate to tissues perinatally, where environmental cues shape their identity and unique functions. Here, we show that the absence of PPARγ affects neonatal development and VCAM-1 expression of splenic iron-recycling red pulp macrophages (RPMs) and bone marrow erythroblastic island macrophages (EIMs). Transcriptome analysis of the few remaining Pparg-deficient RPM-like and EIM-like cells suggests that PPARγ is required for RPM and EIM identity, cell cycling, migration, and localization, but not function in mature RPMs. Notably, Spi-C, another transcription factor implicated in RPM development, was not essential for neonatal expansion of RPMs, even though the transcriptome of Spic-deficient RPMs was strongly affected and indicated a loss of identity. Similarities shared by Pparg- and Spic-deficient RPM-like cells allowed us to identify pathways that rely on both factors. PPARγ and Spi-C collaborate in inducing transcriptional changes, including VCAM-1 and integrin αD expression, which could be required for progenitor retention in the tissue, allowing access to niche-related signals that finalize differentiation.
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What Socratic 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 Socratic graph.