ArticleThe Journal of clinical investigation2023
Monocyte-derived macrophages orchestrate multiple cell-type interactions to repair necrotic liver lesions in disease models.
Article in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 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
58 citing papers in PubMed, 86 citations in OpenAlex.
- Loss of Vacuole Membrane Protein 1 protects against acetaminophen-induced liver injury by modulating inflammation and hepatocyte proliferation.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- MSCs overexpressing FGF21 alleviate acetaminophen-induced acute liver injury by eliciting macrophage-mediated phagocytosis.Hepatology communications · 2026Article
- Reprogramming macrophages to treat liver diseases.Hepatology (Baltimore, Md.) · 2026Review
- Inflammatory monocytes constrain YAP-induced cell proliferation.Science advances · 2026Article
- Therapeutic potential of glycyrrhizic acid in inflammation-related diseases: from HMGB1-oriented molecular insights to preclinical application.Archives of pharmacal research · 2026Review
- TREM1-mediated macrophage activation drives voriconazole-induced hepatic steatosis: Diagnostic and therapeutic implications.Journal of pharmaceutical analysis · 2026Article
- The versatile interplay between steatotic liver disease and liver cancer.Nature reviews. Cancer · 2026Review
- Transient steatosis reprograms MDMs for liver repair.Nature metabolism · 2026Article
- Tumor-associated macrophages promote chemoresistance to Paclitaxel via activating NOTCH2-JAG1 juxtacrine signaling.Molecular cancer · 2026Article
- Cell phenotypic conversion and fate change during the host defense response, tissue injury and repair.Pharmacology & therapeutics · 2026Review
- Unified platform for multiplex immunofluorescence across liver tissues and engineered models.eGastroenterology · 2026Article
- Macrophage duality in liver diseases: heterogeneity, plasticity, and the quest for precision therapeutics.Frontiers in immunology · 2026Review
- Notch signaling in liver diseases: mechanistic insights and therapeutic implications.Frontiers in cell and developmental biology · 2026Review
- ADAM17 as a proteolytic rheostat linking inflammation, tissue repair, and failure of inflammatory resolution in liver injury and fibrosis.Frontiers in pharmacology · 2026Review
- Spatial immune niche remodeling of the neutrophil-macrophage axis inchronic liver disease.Frontiers in cell and developmental biology · 2026Review
- Microbiome-derived bile acids as endogenous regenerative mediators in liver repair.Regenerative therapy · 2025Review
- Liver as a key organ for systemic antimicrobial defense.Hepatology communications · 2025Review
- Hepatic ischemia-reperfusion injury: Underlying mechanisms and concepts in liver surgery and liver transplantation.Hepatology (Baltimore, Md.) · 2025Article
- Adipocyte death promotes hepatic infiltration of S100A8+ macrophages and steatotic liver disease progression in mice.The Journal of clinical investigation · 2025Article
- The spatial and temporal activation of macrophages during fibrosis.Nature reviews. Immunology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 5 institutions in 2 countries.
Funding
Abstract
The liver can fully regenerate after partial resection, and its underlying mechanisms have been extensively studied. The liver can also rapidly regenerate after injury, with most studies focusing on hepatocyte proliferation; however, how hepatic necrotic lesions during acute or chronic liver diseases are eliminated and repaired remains obscure. Here, we demonstrate that monocyte-derived macrophages (MoMFs) were rapidly recruited to and encapsulated necrotic areas during immune-mediated liver injury and that this feature was essential in repairing necrotic lesions. At the early stage of injury, infiltrating MoMFs activated the Jagged1/notch homolog protein 2 (JAG1/NOTCH2) axis to induce cell death-resistant SRY-box transcription factor 9+ (SOX9+) hepatocytes near the necrotic lesions, which acted as a barrier from further injury. Subsequently, necrotic environment (hypoxia and dead cells) induced a cluster of complement 1q-positive (C1q+) MoMFs that promoted necrotic removal and liver repair, while Pdgfb+ MoMFs activated hepatic stellate cells (HSCs) to express α-smooth muscle actin and induce a strong contraction signal (YAP, pMLC) to squeeze and finally eliminate the necrotic lesions. In conclusion, MoMFs play a key role in repairing the necrotic lesions, not only by removing necrotic tissues, but also by inducing cell death-resistant hepatocytes to form a perinecrotic capsule and by activating α-smooth muscle actin-expressing HSCs to facilitate necrotic lesion resolution.
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.