Targeting hepatic macrophages to treat liver diseases
Abstract
Our view on liver macrophages in the context of health and disease has been reformed by the recognition of a remarkable heterogeneity of phagocytes in the liver. Liver macrophages consist of ontogenically distinct populations termed Kupffer cells and monocyte-derived macrophages. Kupffer cells are self-renewing, resident and principally non-migratory phagocytes, serving as sentinels for liver homeostasis. Liver injury triggers Kupffer cell activation, leading to inflammatory cytokine and chemokine release. This fosters the infiltration of monocytes into the liver, which give rise to large numbers of inflammatory monocyte-derived macrophages. Liver macrophages are very plastic and adapt their phenotype according to signals derived from the hepatic microenvironment (e.g. danger signals, fatty acids, phagocytosis of cellular debris), which explains their manifold and even opposing functions during disease. These central functions include the perpetuation of inflammation and hepatocyte injury, activation of hepatic stellate cells with subsequent fibrogenesis, and support of tumor development by angiogenesis and T cell suppression. If liver injury ceases, specific molecular signals trigger hepatic macrophages to switch their phenotype towards reparative phagocytes that promote tissue repair and regression of fibrosis. Novel strategies to treat liver disease aim at targeting macrophages. These interventions modulate Kupffer cell activation (e.g. via gut-liver axis or inflammasome formation), monocyte recruitment (e.g. via inhibiting chemokine pathways like CCR2 or CCL2) or macrophage polarization and differentiation (e.g. by nanoparticles). Evidence from mouse models and early clinical studies in patients with non-alcoholic steatohepatitis and fibrosis support the notion that pathogenic macrophage subsets can be successfully translated into novel treatment options for patients with liver disease. Lay summary Macrophages (Greek for "big eaters") are a frequent non-parenchymal cell type of the liver that ensures homeostasis, antimicrobial defense and proper metabolism. However, liver macrophages consist of different subtypes regarding their ontogeny (developmental origin), differentiation and function. Understanding this heterogeneity and the critical regulation of inflammation, fibrosis and cancer by macrophage subsets opens promising new options for treating liver diseases.
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Macrophages play a central role in regulating liver fibrosis.
“The central role of macrophages in regulating liver fibrosis is now well recognized11,23.”
From Hepatocyte mitochondria-derived danger signals directly activate hepatic stellate cells and drive progression of liver fibrosis (2020) · cites this paper as [23]
Liver macrophages may detect ECM stiffening via mechanotransduction, subsequently differentiating into M1 or M2 phenotypes, leading to the production of cytokines and chemokines and the regulation of HSCs, ultimately influencing the progression and reversal of liver fibrosis.
“Liver macrophages may detect ECM stiffening via mechanotransduction, subsequently differentiating into M1 or M2 phenotypes. This differentiation leads to the production of cytokines and chemokines as well as the regulation of HSCs through intercellular communication, ultimately influencing the progression and reversal of liver fibrosis.”
From Mechanosensitive calcium ion channels Piezo1: A therapeutic target in liver disease (2025) · cites this paper as [76]
There is a significant interaction and interplay between mechanotransduction and biochemical signal transduction within the liver fibrosis process.
“This suggests a significant interaction and interplay between mechanotransduction and biochemical signal transduction within the liver fibrosis process.76,77”
From Mechanosensitive calcium ion channels Piezo1: A therapeutic target in liver disease (2025) · cites this paper as [76]
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- Authors
- Tacke, F.
- Affiliations
- Universitätsklinikum Aachen (DE)
- Corresponding author
- Tacke, Frank
- ORCID
- Tacke, Frank
- Venue
- Journal of Hepatology
- Publisher
- Elsevier BV
- Published
- 2017-06
- Volume
- 66
- Issue
- 6
- Pages
- 1300-1312
- ISSN
- 0168-8278 (ISSN-L)
- OpenAlex
- W2594491387
- Cited by
- 1,003
- References
- 18
- Citations by year
- 2026: 74 · 2025: 124 · 2024: 118 · 2023: 125 · 2022: 149 · 2021: 112 · 2020: 111 · 2019: 91 · 2018: 71 · 2017: 27 · 2013: 1
- FWCI
- 11.83
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Hepatology (publishedVersion)
- PubMed (publishedVersion)
- RWTH Publications (RWTH Aachen) (submittedVersion)
- Funders
- German Research Foundation (Ta434/3-1, Ta434/5-1, SFB/TRR57)
- IZKF
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Keywords
- hepatic macrophages, Kupffer cells, monocyte-derived macrophages, macrophage heterogeneity, liver fibrosis, nonalcoholic steatohepatitis, macrophage polarization, reparative macrophages, liver inflammation, hepatic stellate cells, tumor-associated macrophages, gut-liver axis, inflammasome, chemokine inhibition, CCR2, MCP-1, nanoparticles, liver disease treatment
- MeSH terms
- Animals, Cholestasis, Hepatitis, Viral, Animal, Homeostasis, Humans, Kupffer Cells, Liver Cirrhosis, Liver Diseases, Liver Neoplasms, Experimental, Macrophages, Chemical and Drug Induced Liver Injury
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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