ArticleScientific reports2025
ANGPTL4 induces Kupffer cell M2 polarization to mitigate acute rejection in liver transplantation.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The trial behind it
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Who cites it
8 citing papers in PubMed.
- Arctiin activates CB2R to regulate the TRAF6-STAT1/6 pathway maintain macrophage M1/M2 homeostasis.Journal of molecular histology · 2026Article
- The PPARβ/Delta-Induced Mesenchymal Stromal Cell Secretome Has Cytoprotective Effects via ANGPTL4 in a Pre-Clinical Model of Acute Lung Inflammation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Article
- Circular RNAs in metabolic health: bridging the gap between molecular biology and therapy.Cell death & disease · 2026Review
- Immunopathogenesis of antibody-mediated rejection in liver transplantation.Frontiers in immunology · 2026Review
- Inhibition RIP1 prevents acute liver failure by suppressing hepatic apoptosis and attenuating the secretion of TNF-α from macrophages.European journal of medical research · 2025Article
- ANGPTL4: A Comprehensive Review of 25 Years of Research.Cancers · 2025Review
- Electroacupuncture Attenuates Hepatic Ischemia-Reperfusion Injury by Modulating the Esr1/TAK1-JNK/p38 Signaling Pathway in Rats.Mediators of inflammation · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Acute rejection (AR) is a significant complication in liver transplantation, impacting graft function and patient survival. Kupffer cells (KCs), liver-specific macrophages, can polarize into pro-inflammatory M1 or anti-inflammatory M2 phenotypes, both of which critically influence AR outcomes. Angiopoietin-like 4 (ANGPTL4), a secretory protein, is recognized for its function in regulating inflammation and macrophage polarization. This study investigates the effects of ANGPTL4 on KC polarization through cellular interactions between hepatocytes (HCs) and KCs. Using a rat orthotopic liver transplantation model, we observed reduced ANGPTL4 expression during AR, whereas increased ANGPTL4 levels were linked to immune tolerance. Administration of ANGPTL4 recombinant protein improved liver function, suppressed inflammation, and promoted M2 polarization of KCs. Co-culture experiments demonstrated that hepatocyte-derived ANGPTL4 significantly modulates KC polarization and inflammatory responses, mainly by inhibiting the NF-κB signaling pathway. The results emphasize the promise of ANGPTL4 as a therapeutic target to reduce AR and improve liver transplant outcomes by influencing hepatocyte-KC interactions.
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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.