ArticleThe Journal of biological chemistry2016
Emodin Bidirectionally Modulates Macrophage Polarization and Epigenetically Regulates Macrophage Memory.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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.
The trial behind it
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Who cites it
43 citing papers in PubMed, 79 citations in OpenAlex.
- Anthraquinone-Loaded Liposomes for TAM Reprogramming in Triple-Negative Breast Cancer: Mechanistic Rationale, Delivery Logic, and Translational Challenges.Pharmaceutics · 2026Review
- Discovery and Characterization of Interleukin-4-Specific Affibodies for Affinity-Controlled Protein Release and Macrophage Polarization.bioRxiv : the preprint server for biology · 2026Article
- Emodin and the Anthraquinone Scaffold: Therapeutic Promise and Strategies to Overcome Translational Barriers.Molecules (Basel, Switzerland) · 2026Review
- An Emodin-Depot Microsphere-in-Hydrogel Reprograms the Immuno-myogenic Niche to Enable Volumetric Muscle Loss Repair Revealed by Single-Cell Profiling.Research (Washington, D.C.) · 2026Article
- Barrier Tissue-Resident Macrophages: Natural Compounds as Modulators in Immune Function and Disease.Current topics in medicinal chemistry · 2026Review
- Effect and mechanism of Emodin on mouse myeloid-derived suppressor cells.Frontiers in pharmacology · 2026Article
- Prenylated Dihydroflavonol fromMolecules (Basel, Switzerland) · 2024Article
- Emodin inhibits M1 macrophage activation that related to acute and chronic kidney injury through EGFR/MAPK pathway.Functional & integrative genomics · 2024Article
- Review
- Biological impact and therapeutic implication of tumor-associated macrophages in hepatocellular carcinoma.Cell death & disease · 2024Review
- Panaxynol improves crypt and mucosal architecture, suppresses colitis-enriched microbes, and alters the immune response to mitigate colitis.American journal of physiology. Gastrointestinal and liver physiology · 2024Article
- Review
- Induction of Innate Immune Memory in LPS-Primed Microglial Cells by Water-Soluble Chitosan.BioMed research international · 2024Article
- Therapeutic Potential of 1,8-Dihydroanthraquinone Derivatives for Breast Cancer.International journal of molecular sciences · 2023Review
- H3 histone methylation landscape in male urogenital cancers: from molecular mechanisms to epigenetic biomarkers and therapeutic targets.Frontiers in cell and developmental biology · 2023Review
- Trained immunity in monocyte/macrophage: Novel mechanism of phytochemicals in the treatment of atherosclerotic cardiovascular disease.Frontiers in pharmacology · 2023Review
- Effects of Anthraquinones on Immune Responses and Inflammatory Diseases.Molecules (Basel, Switzerland) · 2022Review
- Emodin suppresses hepatocellular carcinoma growth by regulating macrophage polarization via microRNA-26a/transforming growth factor beta 1/protein kinase B.Bioengineered · 2022Article
- Emodin reduces tumor burden by diminishing M2-like macrophages in colorectal cancer.American journal of physiology. Gastrointestinal and liver physiology · 2022Article
- Mechanism of Emodin in the Treatment of Rheumatoid Arthritis.Evidence-based complementary and alternative medicine : eCAM · 2022Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Macrophages are pleiotropic cells capable of performing a broad spectrum of functions. Macrophage phenotypes are classified along a continuum between the extremes of proinflammatory M1 macrophages and anti-inflammatory M2 macrophages. The seemingly opposing functions of M1 and M2 macrophages must be tightly regulated for an effective and proper response to foreign molecules or damaged tissue. Excessive activation of either M1 or M2 macrophages contributes to the pathology of many diseases. Emodin is a Chinese herb-derived compound and has shown potential to inhibit inflammation in various settings. In this study, we tested the ability of emodin to modulate the macrophage response to both M1 and M2 stimuli. Primary mouse macrophages were stimulated with LPS/IFNγ or IL4 with or without emodin, and the effects of emodin on gene transcription, cell signaling pathways, and histone modifications were examined by a variety of approaches, including microarray, quantitative real-time PCR, Western blotting, chromatin immunoprecipitation, and functional assays. We found that emodin bidirectionally tunes the induction of LPS/IFNγ- and IL4-responsive genes through inhibiting NFκB/IRF5/STAT1 signaling and IRF4/STAT6 signaling, respectively. Thereby, emodin modulates macrophage phagocytosis, migration, and NO production. Furthermore, emodin inhibited the removal of H3K27 trimethylation (H3K27m3) marks and the addition of H3K27 acetylation (H3K27ac) marks on genes required for M1 or M2 polarization of macrophages. In conclusion, our data suggest that emodin is uniquely able to suppress the excessive response of macrophages to both M1 and M2 stimuli and therefore has the potential to restore macrophage homeostasis in various pathologies.
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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.