ArticleHepatology (Baltimore, Md.)2018
Hepatic leukocyte immunoglobulin-like receptor B4 (LILRB4) attenuates nonalcoholic fatty liver disease via SHP1-TRAF6 pathway.
Article in Hepatology (Baltimore, Md.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 53 citations in OpenAlex.
- LILRB4 Recruits SHP-1 to Enhance Oxidative Stress and Apoptosis, Aggravating Myocardial Ischemia-Reperfusion Injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- CD1d functions as a ligand for PIRA2 to drive macrophage activation in nonalcoholic fatty liver disease.Cell death & disease · 2026Article
- Ginsenoside Rg2 upregulates expression of Lilrb4 and inhibits the NF-κB signaling pathway to alleviate hemorrhagic shock/reperfusion-induced intestinal injury.Journal of clinical biochemistry and nutrition · 2026Article
- Syringic Acid in Canarium odontophyllum for Diabetes and Obesity - A Review.Cell biochemistry and biophysics · 2025Review
- Leukocyte immunoglobulin-like receptor B4: A keystone in immune modulation and therapeutic target in cancer and beyond.Cancer innovation · 2024Review
- Microglia LILRB4 upregulation reduces brain damage after acute ischemic stroke by limiting CD8Journal of neuroinflammation · 2024Article
- Effect of Calebin-A on Critical Genes Related to NAFLD: A Protein-Protein Interaction Network and Molecular Docking Study.Current genomics · 2024Article
- Downregulation of LILRB4 Promotes Human Aortic Smooth Muscle Cell Contractile Phenotypic Switch and Apoptosis in Aortic Dissection.Cardiovascular toxicology · 2024Article
- Review
- Discovery of galectin-8 as an LILRB4 ligand driving M-MDSCs defines a class of antibodies to fight solid tumors.Cell reports. Medicine · 2024Article
- Ubiquitination and Metabolic Disease.Advances in experimental medicine and biology · 2024Review
- Molecular and Pathological Analyses of IARS1-Deficient Mice: An IARS Disorder Model.International journal of molecular sciences · 2023Article
- Severe choline deficiency induces alternative splicing aberrance in optimized duck primary hepatocyte cultures.Animal bioscience · 2022Article
- Article
- A targetable LIFR-NF-κB-LCN2 axis controls liver tumorigenesis and vulnerability to ferroptosis.Nature communications · 2021Article
- Anti-NAFLD Effect of Djulis Hull and Its Major Compound, Rutin, in Mice with High-Fat Diet (HFD)-Induced Obesity.Antioxidants (Basel, Switzerland) · 2021Article
- Upregulation of leukocyte immunoglobulin-like receptor B4 on interstitial macrophages in COPD; their possible protective role against emphysema formation.Respiratory research · 2021Article
- Leukocyte immunoglobulin-like receptor subfamily B: therapeutic targets in cancer.Antibody therapeutics · 2021Review
- Macrophage Paired Immunoglobulin-Like Receptor B Deficiency Promotes Peripheral Atherosclerosis in Apolipoprotein E-Deficient Mice.Frontiers in cell and developmental biology · 2021Article
- Protein Arginine Methyltransferase 5 Promotes the Migration of AML Cells by Regulating the Expression of Leukocyte Immunoglobulin-Like Receptor B4.BioMed research international · 2021Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nonalcoholic fatty liver disease (NAFLD) is an increasingly prevalent liver pathology characterized by hepatic steatosis and commonly accompanied by systematic inflammation and metabolic disorder. Despite an accumulating number of studies, no pharmacological strategy is available to treat this condition in the clinic. In this study, we applied extensive gain- and loss-of-function approaches to identify the key immune factor leukocyte immunoglobulin-like receptor B4 (LILRB4) as a negative regulator of NAFLD. The hepatocyte-specific knockout of LILRB4 (LILRB4-HKO) exacerbated high-fat diet-induced insulin resistance, glucose metabolic imbalance, hepatic lipid accumulation, and systematic inflammation in mice, whereas LILRB4 overexpression in hepatocytes showed a completely opposite phenotype relative to that of LILRB4-HKO mice when compared with their corresponding controls. Further investigations of molecular mechanisms demonstrated that LILRB4 recruits SHP1 to inhibit TRAF6 ubiquitination and subsequent inactivation of nuclear factor kappa B and mitogen-activated protein kinase cascades. From a therapeutic perspective, the overexpression of LILRB4 in a genetic model of NAFLD, ob/ob mice, largely reversed the inherent hepatic steatosis, inflammation, and metabolic disorder.
conclusionTargeting hepatic LILRB4 to improve its expression or activation represents a promising strategy for the treatment of NAFLD as well as related liver and metabolic diseases. (Hepatology 2018;67:1303-1319).
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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.