ArticleFrontiers in immunology2020
The Role of Macrophage-Inducible C-Type Lectin in Different Stages of Chronic Liver Disease.
Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Role of macrophages in peritoneal dialysis-associated peritoneal fibrosis.Renal failure · 2025Review
- Gut microbiota and tuberculosis infection: interaction and therapeutic potential.Gut microbes · 2025Review
- New perspectives in the treatment of liver cirrhosis: targeting macrophage regulatory mechanisms.Journal of translational medicine · 2025Review
- Damage-associated molecular patterns (DAMPs) in diseases: implications for therapy.Molecular biomedicine · 2025Review
- Diverse Functions of Macrophages in Obesity and Metabolic Dysfunction-Associated Steatotic Liver Disease: Bridging Inflammation and Metabolism.Immune network · 2025Review
- Mincle as a potential intervention target for the prevention of inflammation and fibrosis (Review).Molecular medicine reports · 2024Review
- Single-cell transcriptome analysis uncovers underlying mechanisms of acute liver injury induced by tripterygium glycosides tablet in mice.Journal of pharmaceutical analysis · 2023Article
- Low lymphocyte-to-monocyte ratio, calcitriol level, and CD206 level predict the development of acute-on-chronic liver failure in patients cirrhosis with acute decompensation.Journal of the Chinese Medical Association : JCMA · 2023Article
- The identification of metabolites from gut microbiota in NAFLD via network pharmacology.Scientific reports · 2023Article
- Dynamic human liver proteome atlas reveals functional insights into disease pathways.Molecular systems biology · 2022Article
- Examination of the role of necroptotic damage-associated molecular patterns in tissue fibrosis.Frontiers in immunology · 2022Review
- BAY61‑3606 attenuates neuroinflammation and neurofunctional damage by inhibiting microglial Mincle/Syk signaling response after traumatic brain injury.International journal of molecular medicine · 2022Article
- ORN: Inferring patient-specific dysregulation status of pathway modules in cancer with OR-gate Network.PLoS computational biology · 2021Article
- Microbiota and Tuberculosis: A Potential Role of Probiotics, and Postbiotics.Frontiers in nutrition · 2021Review
- Roles of Macrophages in the Development and Treatment of Gut Inflammation.Frontiers in cell and developmental biology · 2021Review
- Multiomics Analysis and Machine Learning-based Identification of Molecular Signatures for Diagnostic Classification in Liver Disease Types Along the Microbiota-gut-liver Axis.Journal of clinical and experimental hepatologyArticle
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Authors and funding
19 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The macrophage-inducible C-type lectin (mincle) is part of the innate immune system and acts as a pattern recognition receptor for pathogen-associated molecular patterns (PAMPS) and damage-associated molecular patterns (DAMPs). Ligand binding induces mincle activation which consequently interacts with the signaling adapter Fc receptor, SYK, and NF-kappa-B. There is also evidence that mincle expressed on macrophages promotes intestinal barrier integrity. However, little is known about the role of mincle in hepatic fibrosis, especially in more advanced disease stages. Mincle expression was measured in human liver samples from cirrhotic patients and donors collected at liver transplantation and in patients undergoing bariatric surgery. Human results were confirmed in rodent models of cirrhosis and acute-on-chronic liver failure (ACLF). In these models, the role of mincle was investigated in liver samples as well as in peripheral blood monocytes (PBMC), tissues from the kidney, spleen, small intestine, and heart. Additionally, mincle activation was stimulated in experimental non-alcoholic steatohepatitis (NASH) by treatment with mincle agonist trehalose-6,6-dibehenate (TDB). In human NASH, mincle is upregulated with increased collagen production. In ApoE deficient mice fed high-fat western diet (NASH model), mincle activation significantly increases hepatic collagen production. In human cirrhosis, mincle expression is also significantly upregulated. Furthermore, mincle expression is associated with the stage of chronic liver disease. This could be confirmed in rat models of cirrhosis and ACLF. ACLF was induced by LPS injection in cirrhotic rats. While mincle expression and downstream signaling via FC receptor gamma, SYK, and NF-kappa-B are upregulated in the liver, they are downregulated in PBMCs of these rats. Although mincle expressed on macrophages might be beneficial for intestinal barrier integrity, it seems to contribute to inflammation and fibrosis once the intestinal barrier becomes leaky in advanced stages of chronic liver disease.
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