The DOI matches its Crossref record; 98 of the 98 references it cites were found in a registry or an index.
Resolving the fibrotic niche of human liver cirrhosis at single-cell level
Open accessPublished version of a preprint
Abstract
Liver cirrhosis is a major cause of death worldwide and is characterized by extensive fibrosis. There are currently no effective antifibrotic therapies available. To obtain a better understanding of the cellular and molecular mechanisms involved in disease pathogenesis and enable the discovery of therapeutic targets, here we profile the transcriptomes of more than 100,000 single human cells, yielding molecular definitions for non-parenchymal cell types that are found in healthy and cirrhotic human liver. We identify a scar-associated TREM2+CD9+ subpopulation of macrophages, which expands in liver fibrosis, differentiates from circulating monocytes and is pro-fibrogenic. We also define ACKR1+ and PLVAP+ endothelial cells that expand in cirrhosis, are topographically restricted to the fibrotic niche and enhance the transmigration of leucocytes. Multi-lineage modelling of ligand and receptor interactions between the scar-associated macrophages, endothelial cells and PDGFRα+ collagen-producing mesenchymal cells reveals intra-scar activity of several pro-fibrogenic pathways including TNFRSF12A, PDGFR and NOTCH signalling. Our work dissects unanticipated aspects of the cellular and molecular basis of human organ fibrosis at a single-cell level, and provides a conceptual framework for the discovery of rational therapeutic targets in liver cirrhosis.
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In the citing paper
“Focusing our analysis on the CD4+ T cell compartment, we identified FOXP3+ cells expressing canonical Treg cell transcripts, including IL2RA, CTLA4 and TNFRSF18 (Fig. 1D, right panel).”
From Regulatory T cells safeguard liver health during metabolic-associated steatohepatitis (2026) · cites this paper as [22]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“are equivalent to the scar-associated macrophages (SAM) in human MASH (6–8)”
From Lipid-associated macrophages' promotion of fibrosis resolution during MASH regression requires TREM2 (2024) · cites this paper as [6]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“However, conditioned media from TREM2+ SAM were reported to be more fibrogenic compared to their TREM2− non-scar-associated counterparts (6).”
From Lipid-associated macrophages' promotion of fibrosis resolution during MASH regression requires TREM2 (2024) · cites this paper as [6]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“that are characteristics of SAM described in humans (6, 7).”
From Lipid-associated macrophages' promotion of fibrosis resolution during MASH regression requires TREM2 (2024) · cites this paper as [6]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“The growing accessibility of single-cell transcriptomics has also revealed the presence of numerous subsets/states of macrophages in any given injured tissue in humans (30–33).”
From Targeting macrophages in liver fibrosis (2026) · cites this paper as [31]
Experimental — accuracy not yet measured
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“While the precise roles of the different subsets generated during injury and resolution are still under investigation, the prevailing dogma is that during active fibrogenesis, the macrophage pool is dominated by pro-inflammatory and pro-fibrogenic macrophages (31, 89, 90).”
From Targeting macrophages in liver fibrosis (2026) · cites this paper as [31]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“A good example of this is the population of macrophages in the fibrotic liver, which have been called LAMs, SAMs, and NAMs in different studies, despite largely sharing a conserved transcriptional profile (31, 104, 108).”
From Targeting macrophages in liver fibrosis (2026) · cites this paper as [31]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“these cells also produce mediators such as SPP1 and TGF-β that activate HSCs and hence may promote fibrogenesis (31).”
From Targeting macrophages in liver fibrosis (2026) · cites this paper as [31]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Notably, these cells exhibit a very similar transcriptional profile, with the precise name (LAM, SAM, or NAM) reflecting the different studies in which these cells were identified.”
From Targeting macrophages in liver fibrosis (2026) · cites this paper as [31]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Single-cell RNA-seq studies conducted by independent groups have identified, in human MASLD, macrophage subsets largely analogous to those previously described in mouse (196–198). These include resident KCs (VSIG4+/CD163+/MARCO+/TIMD4+), Mo-KCs (VSIG4+/CD163+/MARCO-/TIMD4-), LAMs (VSIG4-/TREM2+/CD9+) and C-LAMs (VSIG4-/CX3CR1+/CCR2+).”
From Strategies to promote liver fibrosis amelioration with involvement of restorative macrophages (2026) · cites this paper as [198]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“While sub-populations of macrophages and HSCs in the healthy human liver have been described in single-cell data10–12, these subpopulations, and potential gene expression variations within, have not been resolved within the lobule organization at single-cell resolution in the human liver.”
From Spatial transcriptomics of healthy and fibrotic human liver at single-cell resolution (2025) · cites this paper as [11]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“and fibrotic scars (SAM) (6)”
From Lipid-associated macrophages' promotion of fibrosis resolution during MASH regression requires TREM2 (2024) · cites this paper as [6]
The cited source says what the claim attributes to it.
In the citing paper
“On the other hand, those monocytes recruited to zones of steatosis and fibrosis appear to take on an alternative profile, which has been given multiple names, including lipid-associated macrophages (LAMs), scar-associated macrophages (SAMs) and NASH-associated macrophages (NAMs) (31, 104, 108, 109).”
From Targeting macrophages in liver fibrosis (2026) · cites this paper as [31]
The cited source says what the claim attributes to it.
In the citing paper
“Recent single-cell human liver studies have largely focused on chronic liver disease rather than ALF, with emphasis on non-parenchymal cell populations7–9”
From Multimodal decoding of human liver regeneration (2024) · cites this paper as [7]
The cited source says what the claim attributes to it.
In the citing paper
“Notably, TREM2+/CD9+ macrophages have been shown to exhibit a pro-fibrogenic phenotype and to accumulate within collagen-rich fibrotic niches in cirrhotic livers, leading to their designation as scar associated macrophages (SAMs) (198).”
From Strategies to promote liver fibrosis amelioration with involvement of restorative macrophages (2026) · cites this paper as [198]
The cited source says what the claim attributes to it.
In the citing paper
“except for the mere recognition as a marker of fibrosis-associated macrophages39,43–45, the role of TREM2 in regulating the pro-fibrotic AM phenotype in lung fibrosis remains unclear.”
From TREM2 promotes lung fibrosis via controlling alveolar macrophage survival and pro-fibrotic activity (2025) · cites this paper as [39]
The cited source says what the claim attributes to it.
In the citing paper
“In the liver, a TREM2+CD9+ subset of macrophages that differentiate from circulating monocytes expands during liver cirrhosis and contributes to fibrosis (Ramachandran et al., 2019).”
From TREM2 Modulation Remodels the Tumor Myeloid Landscape Enhancing Anti-PD-1 Immunotherapy (2020) · cites this paper as Ramachandran et al., 2019
The cited source says what the claim attributes to it.
In the citing paper
“Both macrophage populations were identified by expression of CD74, while Mac 2 cells also expressed CD5L and MARCO (Fig. 2d, i; Supplementary Fig. 6b), most consistent with non-inflammatory macrophages or Kupffer cells10,11,21.”
From Spatial transcriptomics of healthy and fibrotic human liver at single-cell resolution (2025) · cites this paper as [11]
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Notably, the Treg frequency was significantly elevated in MASH livers relative to that of controls (Fig. 1E), echoing the Treg enrichment observed in the CDAHFD and AMLN models.”
From Regulatory T cells safeguard liver health during metabolic-associated steatohepatitis (2026) · cites this paper as [22]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“PDGFRB expression was concentrated along the edges of ALDOB-expressing hepatocytes in a distribution expected for HSCs, which are located in the subendothelial space11 (Supplementary Fig. 2a–f).”
From Spatial transcriptomics of healthy and fibrotic human liver at single-cell resolution (2025) · cites this paper as [11]
Experimental — accuracy not yet measuredIn the citing paper
“In the cirrhosis-enriched neighbourhoods, we recovered over-expression of known markers of scar-associated endothelium, including ACKR1 and PLVAP (Fig 5F) [2].”
From Differential abundance testing on single-cell data using k-nearest neighbor graphs (2022) · cites this paper as [2]
In the citing paper
“In addition to providing a first-of-its-kind liver cell atlas, this study revealed the presence of two disease-associated endothelial cell populations in the fibrotic niche, characterized as CD34+PLVAP+VWA1+ and CD34+PLVAP+ACKR1+ populations.”
From Inflammation and immunity in liver homeostasis and disease: a nexus of hepatocytes, nonparenchymal cells and immune cells (2025) · cites this paper as [335]
In the citing paper
“Moreover, this same study identified PDGFRA as a marker of scar-associated fibroblasts in cirrhotic livers.”
From Inflammation and immunity in liver homeostasis and disease: a nexus of hepatocytes, nonparenchymal cells and immune cells (2025) · cites this paper as [335]
In the citing paper
“One landmark study described the fibrotic niche in healthy and cirrhotic human livers via single-cell RNA sequencing [335].”
From Inflammation and immunity in liver homeostasis and disease: a nexus of hepatocytes, nonparenchymal cells and immune cells (2025) · cites this paper as [335]
In the citing paper
“ScRNAseq of human cirrhotic livers has identified a subset of TREM2+CD9+ macrophages enriched in heavily scarred regions of the liver that secrete cytokines and growth factors, including epidermal growth factor (EGF) and platelet-derived growth factor BB (PDGF-BB) to create a pro-fibrogenic niche for aHSCs (56).”
From Hepatic Stellate Cell-Immune Interactions in NASH (2022) · cites this paper as [56]
In the citing paper
“This population was found to associate closely with aHSCs and likely overlaps with the scar-associated TREM2+ CD9+ macrophages described by Ramachandran et al. in scRNAseq of human cirrhosis (20, 56).”
From Hepatic Stellate Cell-Immune Interactions in NASH (2022) · cites this paper as [56]
In the citing paper
“Separately, fibrogenic TREM2+CD9+ “scar-associated” macrophages have been characterized in human cirrhosis (56).”
From Hepatic Stellate Cell-Immune Interactions in NASH (2022) · cites this paper as [56]
In the citing paper
“In silico trajectory analysis, based on spliced vs. unspliced mRNA ratios, suggested that these cells were derived from blood monocytes.”
From Understanding the cellular interactome of non-alcoholic fatty liver disease (2022) · cites this paper as [75]
In the citing paper
“Immunofluorescence staining demonstrated that these TREM2+/CD9+ macrophages were highly enriched in the fibrotic niche.”
From Understanding the cellular interactome of non-alcoholic fatty liver disease (2022) · cites this paper as [75]
In the citing paper
“Ramachandran et al. used scRNAseq technology to identify a disease-associated TREM2+/CD9+ macrophage population that was significantly expanded in human cirrhotic livers.”
From Understanding the cellular interactome of non-alcoholic fatty liver disease (2022) · cites this paper as [75]
In the citing paper
“Ligand-receptor pairs were localised to the fibrotic niche between scar-associated macrophages expressing TNFSF12 and PDGFB with myofibroblast receptors TNFSF12A and PDGFRA, respectively.”
From Understanding the cellular interactome of non-alcoholic fatty liver disease (2022) · cites this paper as [75]
In the citing paper
“Gene ontology of the top differentially expressed genes identified pro-fibrogenic factors, such as IL-1B, TREM2 (triggering receptor expressed on myeloid cells 2), CXCR4, C-C motif chemokine receptor (CCR)2, CXCL8, TNFSF12 and vascular endothelial growth factor (VEGF)A, which regulate scar-producing myofibroblasts, upregulate inflammation and promote angiogenesis.”
From Understanding the cellular interactome of non-alcoholic fatty liver disease (2022) · cites this paper as [75]
In the citing paper
“Analysis of the transcriptome of these scar-associated macrophages demonstrated a phenotype analogous to TREM2+/CD9+ BMDMs in mice.”
From Understanding the cellular interactome of non-alcoholic fatty liver disease (2022) · cites this paper as [75]
In the citing paper
“Cognate, pro-fibrotic myofibroblast receptors were also identified for secreted phosphoprotein 1 and IL1β.75”
From Understanding the cellular interactome of non-alcoholic fatty liver disease (2022) · cites this paper as [75]
In the citing paper
“Ramachandran et al. used this approach to identify a distinct population of scar-associated mesenchymal cells in the human liver expressing high levels of fibrogenic genes and the myofibroblast marker, PDGFRA. These myofibroblasts were topographically restricted to fibrotic septae and ligand-receptor analysis revealed a number of pro-fibrogenic pathways including TNFRSF12A, PDGFR and Notch. These”
From Understanding the cellular interactome of non-alcoholic fatty liver disease (2022) · cites this paper as [75]
In the citing paper
“Scar-associated LSECs have been shown by scRNAseq to expand in human cirrhosis. These cells have a PLVAP+ and ACKR1+ transcriptome and demonstrate a number of pro-inflammatory ligand-receptor interactions, such as TGFB1-TGFBR3, JAG1-NOTCH1 and CCL2-ACKR1.75”
From Understanding the cellular interactome of non-alcoholic fatty liver disease (2022) · cites this paper as [75]
In the citing paper
“Seminal work from the Henderson group first profiled hepatic cells, including HSCs from fibrotic mouse and patient livers (50, 51), which has since been expanded to MASH by several other groups including ours.”
From Found in translation—Fibrosis in metabolic dysfunction–associated steatohepatitis (MASH) (2023) · cites this paper as [51]
In the citing paper
“LAMs are identified by the expression of TREM2, Tetraspanin CD9 (CD9), and SPP1, which also represent markers of scar-associated macrophages (SAMs) in cirrhotic patients, suggesting a common macrophage lineage in different liver injury models (51).”
From Found in translation—Fibrosis in metabolic dysfunction–associated steatohepatitis (MASH) (2023) · cites this paper as [51]
In the citing paper
“Animal models implicate HSCs and immune cells, especially macrophages, as major cellular drivers of extracellular matrix turnover, both through reduced secretion of ECM components and crosslinking enzymes as well as increased secretion of proteases and their inhibitors (51, 52, 64, 262, 270-274).”
From Found in translation—Fibrosis in metabolic dysfunction–associated steatohepatitis (MASH) (2023) · cites this paper as [51]
In the citing paper
“Mature and plasma B‐cell clusters have been also detected by sc‐RNAseq within areas of scarring in fibrotic livers of patients with cirrhosis.( 58 )”
From The Emerging Role of B Cells in the Pathogenesis of NAFLD (2021) · cites this paper as [58]
In the citing paper
“While many of these discoveries have been based on mouse models, scRNA-seq analyses from human livers have also identified SAMs as a unique population located in the fibrotic niche of cirrhotic livers of different disease aetiologies.74”
From An integrated view of anti-inflammatory and antifibrotic targets for the treatment of NASH (2023) · cites this paper as [74]
In the citing paper
“Increasingly sophisticated experimental approaches have allowed discovery of significant diversity and functional heterogeneity within the fibroblast population during organ fibrosis22–25 .”
From Fibrosis: from mechanisms to medicines (2020) · cites this paper as [22]
In the citing paper
“a single-cell census of the colonic mesenchyme revealed four subsets of fibroblasts in addition to pericytes and myofibroblasts, and identification of a fibroblast subpopulation proximal to the colonic crypt niche which expressed SOX6, F3 (CD142), and WNT genes essential for colonic epithelial stem cell function.”
From Fibrosis: from mechanisms to medicines (2020) · cites this paper as [22]
In the citing paper
“In colitis, this niche became dysregulated with emergence of an activated mesenchymal population expressing TNFSF14, fibroblastic reticular cell-associated genes, interleukin (IL)-33, and lysyl oxidases (LOX) leading to impaired epithelial proliferation and maturation”
From Fibrosis: from mechanisms to medicines (2020) · cites this paper as [22]
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Self-citation
Metadata
- Authors
- Ramachandran, P., Dobie, R., Wilson-Kanamori, J. R., Dora, E. F., Henderson, B. E. P., Luu, N. T., Portman, J. R., Matchett, K. P., Brice, M., Marwick, J. A., Taylor, R. S., Efremova, M., Vento-Tormo, R., Carragher, N. O., Kendall, T. J., Fallowfield, J. A., Harrison, E. M., Mole, D. J., Wigmore, S. J., Newsome, P. N., Weston, C. J., Iredale, J. P., Tacke, F., Pollard, J. W., Ponting, C. P., Marioni, J. C., Teichmann, S. A., & Henderson, N. C.
- Affiliations
- Centre for Inflammation Research (GB)
- University Hospitals Birmingham NHS Foundation Trust (GB)
- Edinburgh Cancer Research (GB)
- Wellcome Sanger Institute (GB)
- Edinburgh Royal Infirmary (GB)
- National Institute for Health and Care Research (GB)
- Charité – Universitätsmedizin Berlin (DE)
- Albert Einstein College of Medicine (US)
- Institute of Genetics and Cancer (GB)
- European Bioinformatics Institute (GB)
- Corresponding author
- Ramachandran, P.
- Henderson, N. C.
- ORCID
- Ramachandran, P.
- Dobie, R.
- Henderson, B. E. P.
- Luu, N. T.
- Portman, J. R.
- Matchett, K. P.
- Brice, M.
- Taylor, R. S.
- Efremova, M.
- Carragher, N. O.
- Kendall, T. J.
- Fallowfield, J. A.
- Harrison, E. M.
- Mole, D. J.
- Wigmore, S. J.
- Newsome, P. N.
- Weston, C. J.
- Iredale, J. P.
- Tacke, F.
- Pollard, J. W.
- Ponting, C. P.
- Marioni, J. C.
- Teichmann, S. A.
- Henderson, N. C.
- Venue
- Nature
- Published
- 2019-10-09
- Volume
- 575
- Issue
- 7783
- Pages
- 512-518
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC6876711
- OpenAlex
- W2979595830
- Cited by
- 1,784
- References
- 98
- Citations by year
- 2026: 306 · 2025: 319 · 2024: 293 · 2023: 286 · 2022: 220 · 2021: 221 · 2020: 131 · 2019: 7
- FWCI
- 92.30
- Type
- journal article
- Language
- en
- Open access
- green
- doi.org
- Locations
- Nature (publishedVersion)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion, cc-by)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- University of Birmingham Research Portal (University of Birmingham) (submittedVersion)
- Edinburgh Research Explorer (University of Edinburgh) (submittedVersion, other-oa)
- Queen Mary Research Online (Queen Mary University of London) (submittedVersion)
- Bristol Research (University of Bristol) (submittedVersion)
- Apollo (University of Cambridge) (submittedVersion)
- Apollo
- Funders
- Wellcome Trust (RE/18/5/34216, 103749, 101067/Z/13/Z, WT206194, 103749/Z/14/Z)
- University Hospitals Birmingham NHS Foundation Trust
- NIHR Bristol Biomedical Research Centre
- Cancer Research UK (22231)
- National Institute for Health and Care Research
- British Heart Foundation (RM/17/3/33381, RE/18/5/34216)
- Department of Health and Social Care
- Children's Liver Disease Foundation
- Tenovus
- University of Birmingham
- University of Bristol
- Medical Research Council (RM/17/3/33381, MC_PC_15049, MR/N008340/1, 103749, MC_PC_15075, MR/P008887/1, MC_UU_00007/15, MC_PC_15041, RE/18/5/34216, MR/N022556/1)
- Biotechnology and Biological Sciences Research Council (BB/N018869/1, RE/18/5/34216)
- Birmingham Biomedical Research Centre
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Hepatology › Liver Diseases and Immunity
- Health Sciences › Medicine › Hepatology › Liver Disease Diagnosis and Treatment
- Keywords
- liver cirrhosis, liver fibrosis, fibrotic niche, monocyte differentiation, collagen synthesis, TNFRSF12A, Notch signaling, non-parenchymal cells
- MeSH terms
- Animals, Duffy Blood-Group System, Female, Humans, Liver, Liver Cirrhosis, Macrophages, Male, Membrane Glycoproteins, Membrane Proteins, Phenotype, Receptors, Cell Surface, Receptors, Immunologic, Case-Control Studies, Cell Lineage, Receptor, Platelet-Derived Growth Factor alpha, Hepatocytes, Endothelial Cells, Mice, Hepatic Stellate Cells, Transendothelial and Transepithelial Migration, Single-Cell Analysis, Transcriptome, Tetraspanin 29
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