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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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“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]
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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 the citing paper
“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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Metadata
- 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 › Hepatology › 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
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