Macrophage heterogeneity in liver injury and fibrosis
Open accessAbstract
Hepatic macrophages are central in the pathogenesis of chronic liver injury and have been proposed as potential targets in combatting fibrosis. Recent experimental studies in animal models revealed that hepatic macrophages are a remarkably heterogeneous population of immune cells that fulfill diverse functions in homeostasis, disease progression, and regression from injury. These range from clearance of pathogens or cellular debris and maintenance of immunological tolerance in steady state conditions; central roles in initiating and perpetuating inflammation in response to injury; promoting liver fibrosis via activating hepatic stellate cells in chronic liver damage; and, finally, resolution of inflammation and fibrosis by degradation of extracellular matrix and release of anti-inflammatory cytokines. Cellular heterogeneity in the liver is partly explained by the origin of macrophages. Hepatic macrophages can either arise from circulating monocytes, which are recruited to the injured liver via chemokine signals, or from self-renewing embryo-derived local macrophages, termed Kupffer cells. Kupffer cells appear essential for sensing tissue injury and initiating inflammatory responses, while infiltrating Ly-6C(+) monocyte-derived macrophages are linked to chronic inflammation and fibrogenesis. In addition, proliferation of local or recruited macrophages may possibly further contribute to their accumulation in injured liver. During fibrosis regression, monocyte-derived cells differentiate into Ly-6C (Ly6C, Gr1) low expressing 'restorative' macrophages and promote resolution from injury. Understanding the mechanisms that regulate hepatic macrophage heterogeneity, either by monocyte subset recruitment, by promoting restorative macrophage polarization or by impacting distinctive macrophage effector functions, may help to develop novel macrophage subset-targeted therapies for liver injury and fibrosis.
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Recent therapeutic strategies have achieved favorable curative effects by promoting macrophage apoptosis or depleting macrophages.
“recent therapeutic strategies have achieved favorable curative effects by promoting macrophage apoptosis or depleting macrophages.[ 14 ]”
From An Autologous Macrophage‐Based Phenotypic Transformation‐Collagen Degradation System Treating Advanced Liver Fibrosis (2024) · cites this paper as [14]
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- Authors
- Tacke, F., & Zimmermann, H. W.
- Affiliations
- Universitätsklinikum Aachen (DE)
- Corresponding author
- Tacke, Frank
- ORCID
- Tacke, Frank
- Venue
- Journal of Hepatology
- Publisher
- Elsevier BV
- Published
- 2014-05
- Volume
- 60
- Issue
- 5
- Pages
- 1090-1096
- ISSN
- 0168-8278 (ISSN-L)
- OpenAlex
- W1970136916
- Cited by
- 1,061
- References
- 8
- Citations by year
- 2026: 72 · 2025: 93 · 2024: 94 · 2023: 128 · 2022: 115 · 2021: 122 · 2020: 71 · 2019: 78 · 2018: 73 · 2017: 78 · 2016: 69 · 2015: 42 · 2014: 25
- FWCI
- 9.47
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Hepatology (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- RWTH Publications (RWTH Aachen) (submittedVersion)
- Funders
- German Research Foundation (DFG Ta434/2-1, SFB/TRR57)
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Keywords
- hepatic macrophages, macrophage heterogeneity, liver fibrosis, chronic liver injury, Kupffer cells, monocyte-derived macrophages, Ly6C+ monocytes, hepatic stellate cell activation, inflammation resolution, macrophage polarization, macrophage origin, chemokine recruitment, macrophage-targeted therapy
- MeSH terms
- Animals, Cell Differentiation, Humans, Liver, Liver Cirrhosis, Macrophages, Models, Biological, Monocytes, Cell Proliferation, Mice, Translational Research, Biomedical
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