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Mechanisms of Fibrosis Development in Nonalcoholic Steatohepatitis
Open accessAbstract
Nonalcoholic fatty liver disease is the most prevalent liver disease worldwide, affecting 20%-25% of the adult population. In 25% of patients, nonalcoholic fatty liver disease progresses to nonalcoholic steatohepatitis (NASH), which increases the risk for the development of cirrhosis, liver failure, and hepatocellular carcinoma. In patients with NASH, liver fibrosis is the main determinant of mortality. Here, we review how interactions between different liver cells culminate in fibrosis development in NASH, focusing on triggers and consequences of hepatocyte-macrophage-hepatic stellate cell (HSC) crosstalk. We discuss pathways through which stressed and dead hepatocytes instigate the profibrogenic crosstalk with HSC and macrophages, including the reactivation of developmental pathways such as TAZ, Notch, and hedgehog; how clearance of dead cells in NASH via efferocytosis may affect inflammation and fibrogenesis; and insights into HSC and macrophage heterogeneity revealed by single-cell RNA sequencing. Finally, we summarize options to therapeutically interrupt this profibrogenic hepatocyte-macrophage-HSC network in NASH.
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In the citing paper
“The perisinusoidal fibrosis in early human NASH is thought to be produced by activated HSCs/myofibroblasts.114”
From Understanding the cellular interactome of non-alcoholic fatty liver disease (2022) · cites this paper as [114]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“The progression to NASH involves hepatocyte damage and liver inflammation, with the development of liver fibrosis being the key determinant of patient outcomes 3-9 .”
From Amphiregulin from regulatory T cells promotes liver fibrosis and insulin resistance in non-alcoholic steatohepatitis (2024) · cites this paper as [9]
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In the citing paper
“Two independent IM subpopulations that are conserved across lung, fat, heart, and dermis were identified: (Lyve1loMHCIIhiCX3CR1hi (Lyve1loMHCIIhi) and Lyve1hiMHCIIloCX3CR1lo (Lyve1hiMHCIIlo) monocyte-derived IMs.”
From Fibrosis: from mechanisms to medicines (2020) · cites this paper as [61]
Experimental — accuracy not yet measuredIn the citing paper
“The disease-driving pathways of NASH converge in fibrosis (Fig. 3), an aberrant wound-healing process resulting not only in scarring (extracellular matrix deposition), but also in the loss of functional hepatocytes and chronic inflammation.104”
From An integrated view of anti-inflammatory and antifibrotic targets for the treatment of NASH (2023) · cites this paper as [104]
In the citing paper
“The disease-driving pathways of NASH converge in fibrosis (Fig. 3), an aberrant wound-healing process resulting not only in scarring (extracellular matrix deposition), but also in the loss of functional hepatocytes and chronic inflammation.104”
From An integrated view of anti-inflammatory and antifibrotic targets for the treatment of NASH (2023) · cites this paper as [104]
In the citing paper
“Furthermore, monocytes and macrophages are capable of remarkable functional plasticity, displaying diverse phenotypes during wound healing dependent on multiple cues including the environmental niche61,62 and the temporal stage of tissue injury and repair63–66.”
From Fibrosis: from mechanisms to medicines (2020) · cites this paper as [61]
In the citing paper
“demonstrated that the absence of Lyve1hiMHCIIlo IMs exacerbates experimental lung fibrosis, thereby showing that two independent populations of IMs coexist across tissues with conserved niche-dependent functional programs61.”
From Fibrosis: from mechanisms to medicines (2020) · cites this paper as [61]
In the citing paper
“Several recent studies have identified subpopulations of monocytes and macrophages which have the capacity to regulate fibrosis and tissue remodelling18,61,68–71.”
From Fibrosis: from mechanisms to medicines (2020) · cites this paper as [61]
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Citations
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Metadata
- Authors
- Schwabe, R. F., Tabas, I., & Pajvani, U. B.
- Affiliations
- Columbia University Irving Medical Center (US)
- Columbia University (US)
- Corresponding author
- Schwabe, Robert F.
- Venue
- Gastroenterology
- Publisher
- Elsevier BV
- Published
- 2020-05
- Volume
- 158
- Issue
- 7
- Pages
- 1913-1928
- ISSN
- 0016-5085 (ISSN-L)
- PMC
- PMC7682538
- OpenAlex
- W3005214954
- Cited by
- 671
- References
- 169
- Citations by year
- 2026: 82 · 2025: 121 · 2024: 138 · 2023: 131 · 2022: 117 · 2021: 53 · 2020: 27
- FWCI
- 12.15
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Gastroenterology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- Topics
- Health Sciences › Medicine › Hepatology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Hepatology › Liver Diseases and Immunity
- Keywords
- nonalcoholic steatohepatitis, liver fibrosis, hepatic stellate cells, macrophages, hepatocyte death, efferocytosis, TAZ, Notch signaling, Hedgehog signaling, single-cell RNA sequencing, antifibrotic therapy, non-alcoholic fatty liver disease
- MeSH terms
- Animals, Cell Communication, Extracellular Matrix, Humans, Liver, Liver Cirrhosis, Macrophages, Signal Transduction, Cell Death, Hepatocytes, Hepatic Stellate Cells, Non-alcoholic Fatty Liver Disease
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