Heterogeneity of HSCs in a Mouse Model of NASH
Open accessAbstract
Background and Aims: In clinical and experimental NASH, the origin of the scar‐forming myofibroblast is the HSC. We used foz/foz mice on a Western diet to characterize in detail the phenotypic changes of HSCs in a NASH model. Approach and Results: We examined the single‐cell expression profiles (scRNA sequencing) of HSCs purified from the normal livers of foz/foz mice on a chow diet, in NASH with fibrosis of foz/foz mice on a Western diet, and in livers during regression of NASH after switching back to a chow diet. Selected genes were analyzed using immunohistochemistry, quantitative real‐time PCR, and short hairpin RNA knockdown in primary mouse HSCs. Our analysis of the normal liver identified two distinct clusters of quiescent HSCs that correspond to their acinar position of either pericentral vein or periportal vein. The NASH livers had four distinct HSC clusters, including one representing the classic fibrogenic myofibroblast. The three other HSC clusters consisted of a proliferating cluster, an intermediate activated cluster, and an immune and inflammatory cluster. The livers with NASH regression had one cluster of inactivated HSCs, which was similar to, but distinct from, the quiescent HSCs. Conclusions: Analysis of single‐cell RNA sequencing in combination with an interrogation of previous studies revealed an unanticipated heterogeneity of HSC phenotypes under normal and injured states.
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MASH regression is characterized by downregulation of profibrotic and inflammatory genes, HSC inactivation, and resolution of steatosis and fibrosis.
“MASH regression is characterized by downregulation of profibrotic and inflammatory genes, HSC inactivation (31), and resolution of steatosis and fibrosis (22).”
From Lipid-associated macrophages' promotion of fibrosis resolution during MASH regression requires TREM2 (2024) · cites this paper as [31]
The Results section reports that fibrogenic gene expression decreased toward normal after the diet switch, and the Discussion identifies inactivated HSCs during NASH regression. The paper does not establish a general downregulation of inflammatory genes: its Results describe an inflammatory HSC cluster that persists during regression. The separate citation (22) is attached to resolution of steatosis and fibrosis, so that clause is not assessed against this source. Page numbers were not available in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredAbsence of TREM2 impaired effective HSC inactivation, indicated by higher residual αSMA and desmin in Foz::Trem2−/− regressed mice compared to Foz/Foz.
“Absence of TREM2 also impaired effective HSC inactivation (31) indicated by higher residual levels of αSMA (activated HSC marker) and desmin (total HSC marker) in Foz::Trem2−/− regressed mice compared to their Foz/Foz counterparts (Fig. 2H and SI Appendix, Fig. S2B).”
From Lipid-associated macrophages' promotion of fibrosis resolution during MASH regression requires TREM2 (2024) · cites this paper as [31]
The Results and Discussion describe HSC inactivation during NASH regression in foz/foz mice and identify αSMA as an activated-HSC marker and desmin as a general HSC marker (page numbers unavailable). The paper does not report TREM2-deficient mice or compare residual αSMA and desmin levels between Foz::Trem2−/− and Foz/Foz mice, so it cannot support the claimed impairment caused by TREM2 absence. (LLM, conf=0.88)
Experimental — accuracy not yet measuredMASH-associated activated HSCs return to an inactive state during regression that closely resembles quiescent HSCs but is distinct enough to cluster as a separate population.
“In contrast, MASH-associated activated HSCs return to an inactive state during regression, that closely resembles the quiescent HSCs but is distinct enough to cluster as a separate population (31).”
From Lipid-associated macrophages' promotion of fibrosis resolution during MASH regression requires TREM2 (2024) · cites this paper as [31]
Sustained myofibroblast activation in chronic liver disease drives fibrosis, especially in MASH, where myofibroblasts are detectable by desmin and αSMA immunofluorescence and by single-cell RNA-seq gene expression.
“These functions normally contribute to tissue repair under homeostatic conditions, but sustained activation in chronic liver diseases drives fibrosis, especially in MASH (41) where they are detectable by expression of desmin and alpha smooth muscle actin (αSMA) using immunofluorescence, and by conservation of gene expression based on single-cell RNA-seq (42-46).”
From Found in translation—Fibrosis in metabolic dysfunction–associated steatohepatitis (MASH) (2023) · cites this paper as [42]
Although activated HSCs are the primary fibrogenic cells in MASH, single-cell methods have identified an expanded list of fibrogenic drivers expressed by activated HSCs that could be antifibrotic drug targets.
“Although activated HSCs are the primary fibrogenic cells in MASH, these methods have identified an expanded list of fibrogenic drivers expressed by activated HSCs that could represent antifibrotic drug targets (42, 48, 49, 125).”
From Found in translation—Fibrosis in metabolic dysfunction–associated steatohepatitis (MASH) (2023) · cites this paper as [42]
Single-cell studies have revealed heterogeneity within cell types in health and disease, identifying multiple HSC clusters in murine MASH fibrosis and human cirrhosis.
“Single-cell studies have also revealed remarkable heterogeneity within different cell types in health and disease, identifying multiple HSC clusters in murine models of MASH fibrosis and human cirrhosis.”
From Found in translation—Fibrosis in metabolic dysfunction–associated steatohepatitis (MASH) (2023) · cites this paper as [42]
Identification of HSC subpopulations that are the main fibrosis drivers will lead to more targeted, safer therapies.
“3) Identification of HSC subpopulations that are the main fibrosis drivers will lead to more targeted, safer therapies (42, 48).”
From Found in translation—Fibrosis in metabolic dysfunction–associated steatohepatitis (MASH) (2023) · cites this paper as [42]
Single-cell RNA sequencing shows that chemokine/cytokine release and extracellular matrix production vary among HSC/myofibroblast subpopulations because of greater cellular heterogeneity than previously recognised.
“ScRNA-seq allows for high-resolution transcriptomic profiling of mesenchymal subpopulations during liver fibrosis, revealing that chemokine/cytokine release and extracellular matrix production are diversified among HSC/myofibroblast subpopulations owing to a higher degree of cellular heterogeneity than previously appreciated.109–111”
From An integrated view of anti-inflammatory and antifibrotic targets for the treatment of NASH (2023) · cites this paper as [111]
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Cites
Integrating single-cell transcriptomic data across different conditions, technologies, and species
Butler, A., Hoffman, P., Smibert, P., Papalexi, E., & Satija, R. (2018) · Nature Biotechnology · doi:10.1038/nbt.4096 · Cited by 13,174 · see citing works
Trapnell, C., Cacchiarelli, D., Grimsby, J., Pokharel, P., Li, S., Morse, M., Lennon, N. J., Livak, K. J., Mikkelsen, T. S., & Rinn, J. L. (2014) · Nature Biotechnology · doi:10.1038/nbt.2859 · Cited by 7,314 · see citing works
Highly parallel genome-wide expression profiling of individual cells using nanoliter droplets.
Macosko, E. Z., Basu, A., Satija, R., Nemesh, J., Shekhar, K., Goldman, M., Tirosh, I., Bialas, A. R., Kamitaki, N., Martersteck, E. M., et al. (2015) · Cell · doi:10.1016/j.cell.2015.05.002 · Cited by 7,110 · see citing works
Scenic: single-cell regulatory network inference and clustering.
Aibar, S., González-Blas, C. B., Moerman, T., Huynh-Thu, V. A., Imrichova, H., Hulselmans, G., Rambow, F., Marine, J.-C., Geurts, P., Aerts, J., et al. (2017) · Nature Methods · doi:10.1038/nmeth.4463 · Cited by 6,520 · see citing works
Dimensionality reduction for visualizing single-cell data using UMAP
Becht, E., McInnes, L., Healy, J., Dutertre, C.-A., Kwok, I. W. H., Ng, L. G., Ginhoux, F., & Newell, E. W. (2019) · Nature Biotechnology · doi:10.1038/nbt.4314 · Cited by 5,358 · see citing works
La Manno, G., Soldatov, R., Zeisel, A., Braun, E., Hochgerner, H., Petukhov, V., Lidschreiber, K., Kastriti, M. E., Lönnerberg, P., Furlan, A., et al. (2018) · Nature · doi:10.1038/s41586-018-0414-6 · Cited by 4,118 · see citing works
Mechanisms of hepatic stellate cell activation
Tsuchida, T., & Friedman, S. L. (2017) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/nrgastro.2017.38 · Cited by 2,909 · see citing works
Vilar-Gomez, E., Martinez-Perez, Y., Calzadilla-Bertot, L., Torres-Gonzalez, A., Gra-Oramas, B., Gonzalez-Fabian, L., Friedman, S. L., Diago, M., & Romero-Gomez, M. (2015) · Gastroenterology · doi:10.1053/j.gastro.2015.04.005 · Cited by 2,492 · see citing works
Elyada, E., Bolisetty, M., Laise, P., Flynn, W. F., Courtois, E. T., Burkhart, R. A., Teinor, J. A., Belleau, P., Biffi, G., Lucito, M. S., et al. (2019) · Cancer Discovery · doi:10.1158/2159-8290.cd-19-0094 · Cited by 2,241 · see citing works
Resolving the fibrotic niche of human liver cirrhosis at single-cell level
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., et al. (2019) · Nature · doi:10.1038/s41586-019-1631-3 · Cited by 1,784 · see citing works
Single cell RNA sequencing of human liver reveals distinct intrahepatic macrophage populations
MacParland, S. A., Liu, J. C., Ma, X.-Z., Innes, B. T., Bartczak, A. M., Gage, B. K., Manuel, J., Khuu, N., Echeverri, J., Linares, I., et al. (2018) · Nature Communications · doi:10.1038/s41467-018-06318-7 · Cited by 1,552 · see citing works
Mederacke, I., Hsu, C. C., Troeger, J. S., Huebener, P., Mu, X., Dapito, D. H., Pradere, J.-P., & Schwabe, R. F. (2013) · Nature Communications · doi:10.1038/ncomms3823 · Cited by 1,443 · see citing works
Liver inflammation and fibrosis
Koyama, Y., & Brenner, D. A. (2017) · Journal of Clinical Investigation · doi:10.1172/jci88881 · Cited by 1,295 · see citing works
Self-citationA human liver cell atlas reveals heterogeneity and epithelial progenitors
Aizarani, N., Saviano, A., Sagar, Mailly, L., Durand, S., Herman, J. S., Pessaux, P., Baumert, T. F., & Grün, D. (2019) · Nature · doi:10.1038/s41586-019-1373-2 · Cited by 1,147 · see citing works
NLRP3 inflammasome blockade reduces liver inflammation and fibrosis in experimental NASH in mice
Mridha, A. R., Wree, A., Robertson, A. A. B., Yeh, M. M., Johnson, C. D., Van Rooyen, D. M., Haczeyni, F., Teoh, N. C.-H., Savard, C., Ioannou, G. N., et al. (2017) · Journal of Hepatology · doi:10.1016/j.jhep.2017.01.022 · Cited by 1,110 · see citing works
Pancreatic cancer stroma: an update on therapeutic targeting strategies
Hosein, A. N., Brekken, R. A., & Maitra, A. (2020) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/s41575-020-0300-1 · Cited by 950 · see citing works
Myofibroblasts revert to an inactive phenotype during regression of liver fibrosis
Kisseleva, T., Cong, M., Paik, Y., Scholten, D., Jiang, C., Benner, C., Iwaisako, K., Moore-Morris, T., Scott, B., Tsukamoto, H., et al. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1201840109 · Cited by 805 · see citing works
Self-citationXiong, X., Kuang, H., Ansari, S., Liu, T., Gong, J., Wang, S., Zhao, X.-Y., Ji, Y., Li, C., Guo, L., et al. (2019) · Molecular Cell · doi:10.1016/j.molcel.2019.07.028 · Cited by 784 · see citing works
Origin of myofibroblasts in the fibrotic liver in mice
Iwaisako, K., Jiang, C., Zhang, M., Cong, M., Moore-Morris, T. J., Park, T. J., Liu, X., Xu, J., Wang, P., Paik, Y.-H., et al. (2014) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1400062111 · Cited by 535 · see citing works
Self-citationSingle-cell transcriptomics uncovers zonation of function in the mesenchyme during liver fibrosis
Dobie, R., Wilson-Kanamori, J. R., Henderson, B. E. P., Smith, J. R., Matchett, K. P., Portman, J. R., Wallenborg, K., Picelli, S., Zagorska, A., Pendem, S. V., et al. (2019) · Cell Reports · doi:10.1016/j.celrep.2019.10.024 · Cited by 420 · see citing works
Hepatic Free Cholesterol Accumulates in Obese, Diabetic Mice and Causes Nonalcoholic Steatohepatitis
Rooyen, D. M. V., Larter, C. Z., Haigh, W. G., Yeh, M. M., Ioannou, G. N., Kuver, R., Lee, S. P., Teoh, N., & Farrell, G. C. (2011) · Gastroenterology · doi:10.1053/j.gastro.2011.06.040 · Cited by 345 · see citing works
Single-cell technologies in hepatology: new insights into liver biology and disease pathogenesis
Ramachandran, P., Matchett, K. P., Dobie, R., Wilson-Kanamori, J. R., & Henderson, N. C. (2020) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/s41575-020-0304-x · Cited by 253 · see citing works
Krenkel, O., Hundertmark, J., Ritz, T., Weiskirchen, R., & Tacke, F. (2019) · Cells · doi:10.3390/cells8050503 · Cited by 241 · see citing works
Liu, X., Xu, J., Rosenthal, S., Zhang, L., McCubbin, R., Meshgin, N., Shang, L., Koyama, Y., Ma, H., Sharma, S., et al. (2020) · Gastroenterology · doi:10.1053/j.gastro.2020.01.027 · Cited by 205 · see citing works
Self-citationMechanisms Underlying Hepatitis C Virus-Associated Hepatic Fibrosis
Khatun, M., & Ray, R. B. (2019) · Cells · doi:10.3390/cells8101249 · Cited by 187 · see citing works
Arsov, T., Silva, D. G., O’Bryan, M. K., Sainsbury, A., Lee, N. J., Kennedy, C., Manji, S. S. M., Nelms, K., Liu, C., Vinuesa, C. G., et al. (2006) · Molecular Endocrinology · doi:10.1210/me.2005-0494 · Cited by 166 · see citing works
Nishio, T., Hu, R., Koyama, Y., Liang, S., Rosenthal, S. B., Yamamoto, G., Karin, D., Baglieri, J., Ma, H., Xu, J., et al. (2019) · Journal of Hepatology · doi:10.1016/j.jhep.2019.04.012 · Cited by 135 · see citing works
Self-citationCancer-associated fibroblasts: key determinants of tumor immunity and immunotherapy
Barrett, R., & Puré, E. (2020) · Current Opinion in Immunology · doi:10.1016/j.coi.2020.03.004 · Cited by 117 · see citing works
Adaptive failure to high-fat diet characterizes steatohepatitis in Alms1 mutant mice
Arsov, T., Larter, C. Z., Nolan, C. J., Petrovsky, N., Goodnow, C. C., Teoh, N., Yeh, M. M., & Farrell, G. C. (2006) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2006.02.032 · Cited by 113 · see citing works
Migration of Fibrocytes in Fibrogenic Liver Injury
Scholten, D., Reichart, D. R., Paik, Y. H., Lindert, J., Bhattacharya, J., Glass, C. K., Brenner, D. A., & Kisseleva, T. (2011) · American Journal Of Pathology · doi:10.1016/j.ajpath.2011.03.049 · Cited by 107 · see citing works
Self-citationReversibility of Liver Fibrosis and Inactivation of Fibrogenic Myofibroblasts
Liu, X., Xu, J., Brenner, D. A., & Kisseleva, T. (2013) · Current Pathobiology Reports · doi:10.1007/s40139-013-0018-7 · Cited by 106 · see citing works
Self-citationFarrell, G. C., Mridha, A. R., Yeh, M. M., Arsov, T., Van Rooyen, D. M., Brooling, J., Nguyen, T., Heydet, D., Delghingaro‐Augusto, V., Nolan, C. J., et al. (2014) · Liver International · doi:10.1111/liv.12335 · Cited by 85 · see citing works
RNA Velocity: Molecular Kinetics from Single-Cell RNA-Seq
Svensson, V., & Pachter, L. S. (2018) · Molecular Cell · doi:10.1016/j.molcel.2018.09.026 · Cited by 65 · see citing works
Li, X., Su, Y., Hua, X., Xie, C., Liu, J., Huang, Y., Zhou, L., Zhang, M., Li, X., & Gao, Z. (2017) · Journal of Translational Medicine · doi:10.1186/s12967-017-1167-y · Cited by 60 · see citing works
A Single‐Cell Perspective of the Mammalian Liver in Health and Disease
Xiong, X., Kuang, H., Liu, T., & Lin, J. D. (2020) · Hepatology · doi:10.1002/hep.31149 · Cited by 40 · see citing works
Jophlin, L., Koutalos, Y., Chen, C., Shah, V. H., & Rockey, D. C. (2018) · American Journal of Physiology-Gastrointestinal and Liver Physiology · doi:10.1152/ajpgi.00251.2017 · Cited by 33 · see citing works
Role of the Ets-1 Transcription Factor during Activation of Rat Hepatic Stellate Cells in Culture
Knittel, T. E., Kobold, D., Dudás, J., Saile, B., & Ramadori, G. P. (1999) · American Journal Of Pathology · doi:10.1016/s0002-9440(10)65502-2 · Cited by 31 · see citing works
Development of Capsular Fibrosis Beneath the Liver Surface in Humans and Mice
Balog, S., Li, Y., Ogawa, T., Miki, T., Saito, T., French, S. W., & Asahina, K. (2019) · Hepatology · doi:10.1002/hep.30809 · Cited by 28 · see citing works
Flagged first, then by citations
Cited by
Sorted by citations
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Hammerich, L., & Tacke, F. (2023) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/s41575-023-00807-x · Cited by 803 · see citing works
Hepatic fibrosis 2022: Unmet needs and a blueprint for the future
Friedman, S. L., & Pinzani, M. (2022) · Hepatology · doi:10.1002/hep.32285 · Cited by 430 · see citing works
An integrated view of anti-inflammatory and antifibrotic targets for the treatment of NASH
Tacke, F., Puengel, T., Loomba, R., & Friedman, S. L. (2023) · Journal of Hepatology · doi:10.1016/j.jhep.2023.03.038 · Cited by 321 · see citing works
Yang, W., He, H., Wang, T., Su, N., Zhang, F., Jiang, K., Zhu, J., Zhang, C., Niu, K., Wang, L., et al. (2021) · Hepatology · doi:10.1002/hep.31987 · Cited by 250 · see citing works
Found in translation—Fibrosis in metabolic dysfunction–associated steatohepatitis (MASH)
Wang, S., & Friedman, S. L. (2023) · Science Translational Medicine · doi:10.1126/scitranslmed.adi0759 · Cited by 158 · see citing works
Lipid-associated macrophages' promotion of fibrosis resolution during MASH regression requires TREM2
Ganguly, S., Rosenthal, S. B., Ishizuka, K., Troutman, T. D., Rohm, T. V., Khader, N., Aleman-Muench, G., Sano, Y., Archilei, S., Soroosh, P., et al. (2024) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2405746121 · Cited by 145 · see citing works
Self-citationUnderstanding the cellular interactome of non-alcoholic fatty liver disease
Wallace, S. J., Tacke, F., Schwabe, R. F., & Henderson, N. C. (2022) · JHEP Reports · doi:10.1016/j.jhepr.2022.100524 · Cited by 116 · see citing works
Hepatic stellate cells control liver zonation, size and functions via R-spondin 3
Sugimoto, A., Saito, Y., Wang, G., Sun, Q., Yin, C., Lee, K. H., Geng, Y., Rajbhandari, P., Hernandez, C., Steffani, M., et al. (2025) · Nature · doi:10.1038/s41586-025-08677-w · Cited by 110 · see citing works
Neuregulin 4 suppresses NASH-HCC development by restraining tumor-prone liver microenvironment
Zhang, P., Chen, Z., Kuang, H., Liu, T., Zhu, J., Zhou, L., Wang, Q., Xiong, X., Meng, Z., Qiu, X., et al. (2022) · Cell Metabolism · doi:10.1016/j.cmet.2022.07.010 · Cited by 105 · see citing works
Lei, L., Bruneau, A., El Mourabit, H., Guégan, J., Folseraas, T., Lemoinne, S., Karlsen, T. H., Hoareau, B., Morichon, R., Gonzalez‐Sanchez, E., et al. (2022) · Hepatology · doi:10.1002/hep.32456 · Cited by 94 · see citing works
Angiocrine signaling in sinusoidal homeostasis and liver diseases
Gao, J., Lan, T., Kostallari, E., Guo, Y., Lai, E., Guillot, A., Ding, B., Tacke, F., Tang, C., & Shah, V. H. (2024) · Journal of Hepatology · doi:10.1016/j.jhep.2024.05.014 · Cited by 90 · see citing works
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Wiering, L., Subramanian, P., & Hammerich, L. (2023) · Cellular and Molecular Gastroenterology and Hepatology · doi:10.1016/j.jcmgh.2023.02.010 · Cited by 80 · see citing works
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De Smet, V., Eysackers, N., Merens, V., Kazemzadeh Dastjerd, M., Halder, G., Verhulst, S., Mannaerts, I., & van Grunsven, L. A. (2021) · Cell Death & Disease · doi:10.1038/s41419-021-04377-1 · Cited by 78 · see citing works
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Kim, H. Y., Sakane, S., Eguileor, A., Carvalho Gontijo Weber, R., Lee, W., Liu, X., Lam, K., Ishizuka, K., Rosenthal, S. B., Diggle, K., et al. (2024) · Cellular and Molecular Gastroenterology and Hepatology · doi:10.1016/j.jcmgh.2023.09.008 · Cited by 63 · see citing works
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“Using the Foz/Foz model of NASH and regression we recently described the heterogeneity of HSCs within NASH.(36) We also identified the unique gene signature of inactivated HSCs, which was similar to, but distinct from, the quiescent HSCs.”
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- Authors
- Rosenthal, S. B., Liu, X., Ganguly, S., Dhar, D., Pasillas, M. P., Ricciardelli, E., Li, R. Z., Troutman, T. D., Kisseleva, T., Glass, C. K., & Brenner, D. A.
- Affiliations
- University of California San Diego (US)
- Corresponding author
- Brenner, David A.
- ORCID
- Venue
- Hepatology
- Published
- 2021-08
- Volume
- 74
- Issue
- 2
- Pages
- 667-685
- ISSN
- 0270-9139 (ISSN-L)
- 1527-3350
- PMC
- PMC8346581
- OpenAlex
- W3128309898
- Cited by
- 145
- References
- 38
- Citations by year
- 2026: 17 · 2025: 34 · 2024: 27 · 2023: 34 · 2022: 21 · 2021: 12
- FWCI
- 13.32
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Hepatology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Institutes of Health (KL2TR001444)
- National Institute on Alcohol Abuse and Alcoholism (U01AA029019, U01AA022614, U01AA018663, R01AA028550, P50AA011999)
- National Heart, Lung, and Blood Institute (P01HL147835)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK111866, R56DK088837, P30DK120515, P30DK063491, R01DK101737, T32DK007044, R01DK091183, R01DK099205)
- National Institute of Environmental Health Sciences (P42ES010337)
- National Center for Advancing Translational Sciences
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Hepatology › Liver Diseases and Immunity
- Keywords
- hepatic stellate cells, NASH, liver fibrosis, HSC heterogeneity, myofibroblast activation, Western diet, single-cell RNA sequencing, HSC quiescence, hepatic stellate cell activation, liver injury
- MeSH terms
- RNA-Seq, Animals, Cells, Cultured, Disease Models, Animal, Humans, Liver, Male, Mice, Transgenic, Mutation, Genetic Heterogeneity, Cell Cycle Proteins, Mice, Gene Regulatory Networks, Hepatic Stellate Cells, Myofibroblasts, Single-Cell Analysis, Primary Cell Culture, Non-alcoholic Fatty Liver Disease, Diet, Western
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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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