Hepatocyte Notch activation induces liver fibrosis in nonalcoholic steatohepatitis
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Aberrant hepatocyte Notch activation is required for development of NASH-associated fibrosis, and Notch inhibition ameliorates obesity-induced liver disease.
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Cholesterol and other mediators contribute to changes in transcriptional programmes in steatotic hepatocytes, leading to upregulation of developmental pathways such as Notch and TAZ, which can directly activate pro-fibrotic cell-cell communication between hepatocytes and neighbouring cells.
“In parallel, cholesterol and other mediators contribute to changes in the transcriptional programmes in steatotic hepatocytes, leading to an upregulation of developmental pathways that are often seen in bipotential progenitor cells or ductular cells, such as Notch and TAZ, which can directly activate pro-fibrotic cell-cell communication between hepatocytes and neighbouring cells.[28], [29], [30]”
From Understanding the cellular interactome of non-alcoholic fatty liver disease (2022) · cites this paper as [29]
Osteopontin is induced by Notch and TAZ signalling.
“osteopontin, which is induced by Notch and TAZ signalling129”
From Understanding the cellular interactome of non-alcoholic fatty liver disease (2022) · cites this paper as [129]
Blocking notch signaling in MASH, genetically or pharmacologically, can attenuate MASH-associated liver fibrosis.
“Blocking notch signaling in MASH, both genetically and pharmacologically, can attenuate MASH-associated liver fibrosis (114).”
From Found in translation—Fibrosis in metabolic dysfunction–associated steatohepatitis (MASH) (2023) · cites this paper as [114]
Notch signaling is an important driver of HSC activation in fibrosis generally.
“Notch signaling has been identified as an important driver of HSC activation in fibrosis in general (114, 153).”
From Found in translation—Fibrosis in metabolic dysfunction–associated steatohepatitis (MASH) (2023) · cites this paper as [114]
In hepatocytes, TLR4 activation increases JAG1, leading to SOX9-dependent transcription and SPP1 secretion, which stimulates HSC activation.
“In hepatocytes, activation of TLR4 increases the expression of jagged 1 (JAG1), a well-established notch receptor 1 (NOTCH1) ligand, which leads to SRY-box transcription factor 9 (SOX9)-dependent transcription and secretion of SPP1, stimulating HSC activation (114).”
From Found in translation—Fibrosis in metabolic dysfunction–associated steatohepatitis (MASH) (2023) · cites this paper as [114]
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- Authors
- Zhu, C., Kim, K., Wang, X., Bartolome, A., Salomao, M., Dongiovanni, P., Meroni, M., Graham, M. J., Yates, K. P., Diehl, A. M., Schwabe, R. F., Tabas, I., Valenti, L., Lavine, J. E., & Pajvani, U. B.
- Affiliations
- Columbia University (US)
- Department of Medicine, Columbia University, New York, NY 10032, USA.
- Mayo Clinic (US)
- University of Milan (IT)
- Ionis Pharmaceuticals (United States) (US)
- Johns Hopkins University (US)
- Duke Medical Center (US)
- Corresponding author
- Pajvani, Utpal B.
- ORCID
- Venue
- Science Translational Medicine
- Published
- 2018-11-21
- Volume
- 10
- Issue
- 468
- ISSN
- 1946-6234 (ISSN-L)
- 1946-6242
- PMC
- PMC6822168
- OpenAlex
- W2901663946
- Cited by
- 250
- References
- 78
- Citations by year
- 2026: 19 · 2025: 40 · 2024: 41 · 2023: 40 · 2022: 31 · 2021: 43 · 2020: 29 · 2019: 7
- FWCI
- 12.37
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science Translational Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (acceptedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (DK103818, DK105303)
- 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
- Notch signaling, hepatocytes, liver fibrosis, nonalcoholic steatohepatitis, antifibrotic therapy, diet-induced liver disease
- MeSH terms
- Animals, Choline, Diet, Female, Humans, Liver Cirrhosis, Male, Methionine, Mice, Inbred C57BL, Hepatocytes, Receptors, Notch, Osteopontin, Hepatic Stellate Cells, SOX9 Transcription Factor, Non-alcoholic Fatty Liver Disease
About these checks
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.
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