Fate tracing reveals hepatic stellate cells as dominant contributors to liver fibrosis independent of its aetiology
Open accessAbstract
Although organ fibrosis causes significant morbidity and mortality in chronic diseases, the lack of detailed knowledge about specific cellular contributors mediating fibrogenesis hampers the design of effective antifibrotic therapies. Different cellular sources, including tissue-resident and bone marrow-derived fibroblasts, pericytes and epithelial cells, have been suggested to give rise to myofibroblasts, but their relative contributions remain controversial, with profound differences between organs and different diseases. Here we employ a novel Cre-transgenic mouse that marks 99% of hepatic stellate cells (HSCs), a liver-specific pericyte population, to demonstrate that HSCs give rise to 82-96% of myofibroblasts in models of toxic, cholestatic and fatty liver disease. Moreover, we exclude that HSCs function as facultative epithelial progenitor cells in the injured liver. On the basis these findings, HSCs should be considered the primary cellular target for antifibrotic therapies across all types of liver disease.
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Besides hepatic stellate cells, portal fibroblasts, bone marrow-derived fibrocytes, and MSCs contribute to the pool of myofibroblasts to a minor extent.
“Besides HSCs, other cells, including portal fibroblasts (particularly in cholestatic liver fibrosis), bone marrow-derived fibrocytes, and MSCs contribute to the pool of MFs as well, albeit to a minor extent [7, 13].”
From Mechanisms, efficacy, and future perspectives of cellular-based therapies for liver fibrosis/cirrhosis: focusing on mesenchymal stromal cells (2025) · cites this paper as [13]
The Introduction says bone marrow-derived fibrocytes may contribute to the myofibroblast pool to a lesser degree. The Results identify a small population of portal fibroblast-like myofibroblasts in cholestatic fibrosis, and the Discussion says they are less abundant than HSCs. Our copy does not identify MSCs as contributors, so that part of the claim is unsupported (searched: MSC, mesenchymal stem cells). (LLM, conf=0.85)
Experimental — accuracy not yet measuredHepatic stellate cells are the predominant (>95%) source of collagen-producing cells and myofibroblasts in liver fibrosis.
“hepatic stellate cells, the predominant (>95%) source of collagen-producing cells and myofibroblasts in liver fibrosis 15,43 .”
From Amphiregulin from regulatory T cells promotes liver fibrosis and insulin resistance in non-alcoholic steatohepatitis (2024) · cites this paper as [15]
The Results (page unavailable in our copy) identify hepatic stellate cells as the dominant source of collagen-producing cells and myofibroblasts in the liver-fibrosis models studied. The >95% figure does not hold across those models: the paper reports 96.0% overlap with collagen-producing cells in one toxic-fibrosis model, but 82–85% of collagen-producing cells and 80–88% overlap with myofibroblast markers in biliary fibrosis. (LLM, conf=0.92)
Experimental — accuracy not yet measuredIn the fibrotic liver, activated hepatic stellate cells are the predominant source (>80%) of myofibroblasts.
“In the fibrotic liver, activated HSCs (aHSCs) have been identified as the predominant source (> 80%) of MFs [7, 13].”
From Mechanisms, efficacy, and future perspectives of cellular-based therapies for liver fibrosis/cirrhosis: focusing on mesenchymal stromal cells (2025) · cites this paper as [13]
Hepatic stellate cells are central to liver fibrosis.
“Hepatic stellate cells - liver-resident fibroblasts - are central to liver fibrosis 15 and interplay with hepatocytes via cell-cell contact and soluble mediators that support hepatocyte development and homeostasis 16,17 .”
From Amphiregulin from regulatory T cells promotes liver fibrosis and insulin resistance in non-alcoholic steatohepatitis (2024) · cites this paper as [15]
Following injury, HSCs undergo a well-characterized activation process and become the primary fibrogenic cell type of the liver.
“Following injury, HSCs undergo a well-characterized activation process and become the primary fibrogenic cell type of the liver [221, 227, 228].”
From Inflammation and immunity in liver homeostasis and disease: a nexus of hepatocytes, nonparenchymal cells and immune cells (2025) · cites this paper as [227]
Fibrogenesis is driven by myofibroblasts originating mainly from hepatic stellate cells and portal fibroblasts that acquire fibrogenic, proliferative, immunomodulatory, contractile, and angiogenic properties in response to liver injury.
“Fibrogenesis is driven by myofibroblasts, originating mainly from hepatic stellate cells (HSCs) and portal fibroblasts (3, 4) that acquire fibrogenic, proliferative, immunomodulatory, contractile, and angiogenic properties in response to liver injury (1, 5).”
From Immunoregulation of Liver Fibrosis: New Opportunities for Antifibrotic Therapy (2024) · cites this paper as [4]
In rodent models of parenchymal injury, it is predominantly HSCs that activate and differentiate into myofibroblasts.
“In rodent models of parenchymal injury, it is predominantly HSCs that activate and differentiate into myofibroblasts.112,113”
From Understanding the cellular interactome of non-alcoholic fatty liver disease (2022) · cites this paper as [113]
Most myofibroblasts in chemically injured mouse models come from HSCs, and depleting them reduces liver fibrosis.
“The majority of myofibroblasts in chemically-injured mouse models also derive from HSCs, and their depletion reduces liver fibrosis (52-54).”
From Found in translation—Fibrosis in metabolic dysfunction–associated steatohepatitis (MASH) (2023) · cites this paper as [53]
Other myofibroblast sources include vascular smooth muscle cells, mesothelial cells, and portal fibroblasts; portal myofibroblasts marked by THY1 may play an outsized role in biliary fibrosis because of their portal location.
“Other sources of myofibroblasts include vascular smooth muscle cells, mesothelial cells, and portal fibroblasts, out of which portal myofibroblasts marked by thymocyte differentiation antigen 1 (THY1) may play an outsized role in biliary fibrosis due to their physical localization in the portal region (53, 55-57) (58).”
From Found in translation—Fibrosis in metabolic dysfunction–associated steatohepatitis (MASH) (2023) · cites this paper as [53]
The primary cellular driver of liver fibrogenesis is activated hepatic stellate cells.
“The primary cellular driver of liver fibrogenesis is activated hepatic stellate cells.”
From Nuclear receptors in liver fibrosis (2021) · cites this paper as [6]
Activated hepatic stellate cells represent the main source of fibrogenic myofibroblasts.
“While aHSCs represent the main source of fibrogenic MFs, [6]”
From Nuclear receptors in liver fibrosis (2021) · cites this paper as [6]
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- Authors
- Mederacke, I., Hsu, C. C., Troeger, J. S., Huebener, P., Mu, X., Dapito, D. H., Pradere, J.-P., & Schwabe, R. F.
- Affiliations
- Columbia University (US)
- Corresponding author
- Schwabe, Robert F.
- Venue
- Nature Communications
- Published
- 2013-11-22
- Volume
- 4
- Issue
- 1
- Pages
- 2823-2823
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC4059406
- OpenAlex
- W1965588383
- Cited by
- 1,443
- References
- 56
- Citations by year
- 2026: 111 · 2025: 126 · 2024: 121 · 2023: 194 · 2022: 136 · 2021: 116 · 2020: 124 · 2019: 101 · 2018: 97 · 2017: 91 · 2016: 80 · 2015: 85 · 2014: 53 · 2013: 3 · 2012: 2
- FWCI
- 45.87
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Nature Communications (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- American Liver Foundation (ME 3723/1-1, 1F31DK091980)
- Case Western Reserve University
- Deutsche Forschungsgemeinschaft (1F31DK091980, ME 3723/1-1)
- National Institutes of Health
- University of California, San Diego
- National Cancer Institute (U54CA163111)
- National Institute of Diabetes and Digestive and Kidney Diseases (5R01DK76920, R01DK076920, F31DK091980, R01DK075830)
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
- Keywords
- hepatic stellate cells, liver fibrosis, myofibroblast origin, fibrogenesis, toxic liver injury, cholestatic liver disease, hepatic steatosis, antifibrotic therapy, bone marrow-derived fibroblasts, pericytes, epithelial progenitor cells
- MeSH terms
- Animals, Female, Liver Cirrhosis, Male, Mice, Inbred CBA, Mice, Inbred C57BL, Genes, Reporter, Integrases, Mice, Hepatic Stellate Cells, Myofibroblasts
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