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Liver fibrosis
Open accessAbstract
Liver fibrosis is the excessive accumulation of extracellular matrix proteins including collagen that occurs in most types of chronic liver diseases. Advanced liver fibrosis results in cirrhosis, liver failure, and portal hypertension and often requires liver transplantation. Our knowledge of the cellular and molecular mechanisms of liver fibrosis has greatly advanced. Activated hepatic stellate cells, portal fibroblasts, and myofibroblasts of bone marrow origin have been identified as major collagen-producing cells in the injured liver. These cells are activated by fibrogenic cytokines such as TGF-beta1, angiotensin II, and leptin. Reversibility of advanced liver fibrosis in patients has been recently documented, which has stimulated researchers to develop antifibrotic drugs. Emerging antifibrotic therapies are aimed at inhibiting the accumulation of fibrogenic cells and/or preventing the deposition of extracellular matrix proteins. Although many therapeutic interventions are effective in experimental models of liver fibrosis, their efficacy and safety in humans is unknown. This review summarizes recent progress in the study of the pathogenesis and diagnosis of liver fibrosis and discusses current antifibrotic strategies.
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“The current study amends this fibrocentric concept by demonstrating fibrosis-independent roles for HSCs through RSPO3, regulating critical parameters that affect CLD progression and outcomes, including metabolic hepatocyte functions, liver regeneration and hepatocyte death2,49,50.”
From Hepatic stellate cells control liver zonation, size and functions via R-spondin 3 (2025) · cites this paper as [2]
In the citing paper
“In more advanced disease stages, the ECM can replace functional liver parenchyma and thereby contribute to the development of liver cirrhosis, which is characterized by bridging fibrosis, regenerative nodules, and the loss of liver function [230].”
From Inflammation and immunity in liver homeostasis and disease: a nexus of hepatocytes, nonparenchymal cells and immune cells (2025) · cites this paper as [230]
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“Two of the prototype cytokines responsible for the activation of HSCs during liver injury are the transforming growth factor-β (TGF-β) and the platelet-derived growth factor (PDGF).[3]”
From Nuclear receptors in liver fibrosis (2021) · cites this paper as [3]
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Metadata
- Authors
- Bataller, R., & Brenner, D. A.
- Affiliations
- Columbia University (US)
- Corresponding author
- Brenner, David A.
- ORCID
- Brenner, David A.
- Venue
- Journal of Clinical Investigation
- Published
- 2005-02-01
- Volume
- 115
- Issue
- 2
- Pages
- 209-218
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W4255712601
- Cited by
- 4,958
- References
- 134
- Citations by year
- 2026: 177 · 2025: 236 · 2024: 285 · 2023: 289 · 2022: 307 · 2021: 321 · 2020: 294 · 2019: 275 · 2018: 284 · 2017: 295 · 2016: 281 · 2015: 307 · 2014: 229 · 2013: 224 · 2012: 222
- FWCI
- 17.47
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Ministerio de Ciencia y Tecnología
- National Institutes of Health
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Hepatology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Hepatology › Liver Disease and Transplantation
- Keywords
- liver fibrosis, extracellular matrix accumulation, collagen deposition, chronic liver disease, liver cirrhosis, hepatic stellate cells, portal fibroblasts, myofibroblasts, TGF-β1, angiotensin II, leptin, fibrogenic cytokines, antifibrotic agents, fibrosis pathogenesis, fibrosis diagnosis, liver transplantation
- MeSH terms
- Angiotensin II, Animals, Humans, Hypertension, Portal, Liver Cirrhosis, Transforming Growth Factor beta, Liver Failure, Leptin
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