ArticleJournal of clinical and translational hepatology2023
IGF2-NR4A2 Signaling Regulates Macrophage Subtypes to Attenuate Liver Cirrhosis.
Article in Journal of clinical and translational hepatology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 2 of them syntheses that pooled it.
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
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
11 citing papers in PubMed, 2 syntheses or guidelines pooled it, 14 citations in OpenAlex.
- The diagnostic accuracy of MMP-7 for the diagnosis for biliary atresia- a systematic review and meta-analysis.BMC pediatrics · 2025Pooled it
- Effect of serum MMP-7 on the diagnostic accuracy of biliary atresia: systematic review and meta-analysis.Frontiers in pharmacology · 2025Pooled it
- Harnessing macrophage signaling pathways and scalable engineering for next-generation immunotherapies.Signal transduction and targeted therapy · 2026Review
- Insulin-Like Growth Factor 2 Modulates Macrophage Polarization: the Role of the IGF2-IGFBP6 Axis.Doklady. Biochemistry and biophysics · 2026Article
- Ultra-Large Spontaneous Portosystemic Shunt is Correlated With a Higher Hepatic Venous Pressure Gradient and Increased Risk of Hepatic Encephalopathy.Canadian journal of gastroenterology & hepatology · 2026Article
- Bifunctional adECM bioscaffold with STIM1-ASCs and IGF-2 promotes functional masseter VML repair via myogenesis and fibrosis suppression.Bioactive materials · 2025Article
- Nurr1 attenuates hepatic stellate cell activation by inhibiting EMT and cell cycle progression via interaction with Smad3.Molecular biology reports · 2025Article
- CCNE1 Promotes the Progression of Hepatic Precancerous Lesion and the Malignant Phenotype of Hepatocellular Carcinoma.Journal of clinical and translational hepatology · 2025Article
- Paradoxical regulation of IGF2 in promoting lipid metabolism in adipose tissues.Communications biology · 2025Article
- IGF2-Reprogrammed Macrophages Ameliorate the Inflammatory Response and Protect Against the Neuroinflammatory Process in Parkinson's Disease Models.Aging cell · 2025Article
- Progress in Biomarkers Related to Biliary Atresia.Journal of clinical and translational hepatology · 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
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background and Aims: Liver cirrhosis can lead to liver failure and eventually death. Macrophages are the main contributors to cirrhosis and have a bidirectional role in regulating matrix deposition and degradation. Macrophage-based cell therapy has been developed as an alternative to liver transplantation. However, there is insufficient evidence regarding its safety and efficacy. In this study, we aimed to explore the effect of combining insulin-like growth factor 2 (IGF2) with bone marrow-derived macrophages (BMDMs) to treat mice with liver cirrhosis. Methods: We assessed liver inflammation, fibrosis regression, liver function, and liver regeneration in mice with CCl Results: Combining IGF2 with BMDM reduced liver inflammation and fibrosis and increased hepatocyte proliferation. Combining IGF2 with BMDM was more effective than using BMDM alone. Conclusions: Our study provides a theoretical basis for the future use of BMDM-based cell therapy to treat liver cirrhosis.
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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.