Monocyte-derived Kupffer cells dominate in the Kupffer cell pool during liver injury
Open accessAbstract
Healthy Kupffer cell (KC) pool is dominated by embryonic KCs (EmKCs), preserving liver homeostasis. How the KC pool varies upon injury remains unclear. Using chimeric mice with bone marrow (BM) cells labeled with enhanced green fluorescent protein, we identify that BM monocyte-derived KCs (MoKCs) become dominant in cholestatic- or toxic-injured livers via immunofluorescence and mass cytometry. Single-cell RNA sequencing (scRNA-seq) unveils the enhanced proliferative, anti-apoptotic properties and repair potential of MoKCs compared with EmKCs, which are confirmed in vivo and ex vivo through flow cytometry, qPCR, Cell Counting Kit-8, and immunofluorescence. Furthermore, compared with EmKC-dominated livers, MoKC-dominated livers exhibit less functional damage, necrosis, and fibrosis under damage, as tested by serum alanine aminotransferase activity detection, H&E and Sirius red staining, qPCR, and western blot. Collectively, we highlight that MoKCs dominate the KC pool in injured livers and show enhanced proliferative and anti-apoptotic properties while also promoting repair and attenuating fibrosis.
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Monocyte-derived Kupffer cells exhibit a distinct transcriptional repertoire characterized by enhanced expression of genes for tissue repair, matrix remodeling, and phagocytosis, translating into stronger phagocytic capacity and greater ability to attenuate liver fibrosis in vivo.
“MoKCs exhibit a distinct transcriptional repertoire characterized by enhanced expression of genes for tissue repair, matrix remodeling, and phagocytosis, translating into stronger phagocytic capacity and greater ability to attenuate liver fibrosis in vivo (38).”
From Macrophage duality in liver diseases: heterogeneity, plasticity, and the quest for precision therapeutics (2026) · cites this paper as [38]
The replacement of Kupffer cells by monocyte-derived Kupffer cells represents functional upgrading, not mere substitution.
“Crucially, this replacement represents functional upgrading, not mere substitution.”
From Macrophage duality in liver diseases: heterogeneity, plasticity, and the quest for precision therapeutics (2026) · cites this paper as [38]
In cholestatic and toxic models, recruited Ly6C+ monocytes differentiate into monocyte-derived Kupffer cells that rapidly dominate the Kupffer cell pool due to enhanced proliferation and anti-apoptotic properties.
“For example, in cholestatic and toxic models, recruited Ly6C+ monocytes differentiate into monocyte-derived KCs (MoKCs) that, due to enhanced proliferation and anti-apoptotic properties, rapidly dominate the KC pool.”
From Macrophage duality in liver diseases: heterogeneity, plasticity, and the quest for precision therapeutics (2026) · cites this paper as [38]
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References 48 · Cited by 74
- Authors
- Li, W., Yang, Y., Yang, L., Chang, N., & Li, L.
- Affiliations
- Capital Medical University (CN)
- Corresponding author
- Chang, Na
- Li, Liying
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2023-10
- Volume
- 42
- Issue
- 10
- Pages
- 113164
- ISSN
- 2211-1247 (ISSN-L)
- OpenAlex
- W4386993734
- Cited by
- 74
- References
- 48
- Citations by year
- 2026: 25 · 2025: 36 · 2024: 13
- FWCI
- 12.53
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cell Reports (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Natural Science Foundation of China (81430013, 81770603, 81970532, 82170622)
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Keywords
- Kupffer cells, liver injury, cholestasis, hepatotoxicity, Kupffer cell proliferation, liver repair, liver fibrosis, chimeric mice
- MeSH terms
- Animals, Fibrosis, Kupffer Cells, Liver, Monocytes, Necrosis, Mice
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