The DOI matches its Crossref record; 112 of the 112 references it cites were found in a registry or an index.
Liver fibrosis and hepatic stellate cells: Etiology, pathological hallmarks and therapeutic targets
Open accessAbstract
Liver fibrosis is a reversible wound-healing process aimed at maintaining organ integrity, and presents as the critical pre-stage of liver cirrhosis, which will eventually progress to hepatocellular carcinoma in the absence of liver transplantation.Fibrosis generally results from chronic hepatic injury caused by various factors, mainly viral infection, schistosomiasis, and alcoholism; however, the exact pathological mechanisms are still unknown.Although numerous drugs have been shown to have antifibrotic activity in vitro and in animal models, none of these drugs have been shown to be efficacious in the clinic.Importantly, hepatic stellate cells (HSCs) play a key role in the initiation, progression, and regression of liver fibrosis by secreting fibrogenic factors that encourage portal fibrocytes, fibroblasts, and bone marrow-derived myofibroblasts to produce collagen and thereby propagate fibrosis.These cells are subject to intricate cross-talk with adjacent cells, resulting in scarring and subsequent liver damage.Thus, an understanding of the molecular mechanisms of liver fibrosis and their relationships with HSCs is essential for the discovery of new therapeutic targets.This comprehensive review outlines the role of HSCs in liver fibrosis and details novel strategies to suppress HSC activity, thereby providing new insights into potential treatments for liver fibrosis.
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“Hepatic stellate cells, characterized by DES and VIM expressions, are central to liver fibrosis and extracellular matrix remodeling34,36.”
From Temporal proteomic profiling of iPSC-derived human liver organoids reveals optimal maturation for drug metabolism and toxicology (2026) · cites this paper as [34]
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“Interestingly, the mesenchymal shift by Day 45 suggests greater cellular complexity at later stages, potentially facilitating iHLO use in modeling liver pathologies such as fibrosis, cirrhosis, and liver remodeling, as indicated by increased expression of hepatic stellate cell markers such as DES and VIM33,34.”
From Temporal proteomic profiling of iPSC-derived human liver organoids reveals optimal maturation for drug metabolism and toxicology (2026) · cites this paper as [34]
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“The expansion of mesenchymal-like population at Day 45 suggests that these organoids could serve as an advanced model for studying fibrogenesis and testing anti-fibrotic therapies34.”
From Temporal proteomic profiling of iPSC-derived human liver organoids reveals optimal maturation for drug metabolism and toxicology (2026) · cites this paper as [34]
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Resveratrol improves health and survival of mice on a high-calorie diet
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The burden of liver disease in Europe: A review of available epidemiological data
Blachier, M., Leleu, H., Peck‐Radosavljevic, M., Valla, D. C., & Roudot‐Thoraval, F. (2013) · Journal of Hepatology · doi:10.1016/j.jhep.2012.12.005 · Cited by 1,340
The natural history of nonalcoholic fatty liver: A follow-up study
Teli, M. R., James, O., Burt, A. D., Bennett, M. K., & Day, C. P. (1995) · Hepatology · doi:10.1002/hep.1840220616 · Cited by 913
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CYP2E1 and oxidative liver injury by alcohol
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Hepatic fibrosis: concept to treatment
Trautwein, C., Friedman, S. L., Schuppan, D., & Pinzani, M. (2015) · Journal of Hepatology · doi:10.1016/j.jhep.2015.02.039 · Cited by 677
AMP-activated protein kinase-deficient mice are resistant to the metabolic effects of resveratrol
Um, J.-H., Park, S.-J., Kang, H., Yang, S., Foretz, M., McBurney, M. W., Kim, M. K., Viollet, B., & Chung, J. H. (2010) · Diabetes · doi:10.2337/db09-0482 · Cited by 647
Research works printed but not linked: 1
- 10.1002/cphy.c120035 · DOI · Paper page
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Wound healing, fibroblast heterogeneity, and fibrosis
desJardins-Park, H. E., Mascharak, S., Griffin, M., Wan, D. C., & Longaker, M. T. (2022) · Cell stem cell · doi:10.1016/j.stem.2022.07.006 · Cited by 835
Dilliard, S. A., & Siegwart, D. J. (2023) · Nature Reviews Materials · doi:10.1038/s41578-022-00529-7 · Cited by 744
Aydin, M. M., & Akçalı, K. C. (2018) · The Turkish Journal of Gastroenterology · doi:10.5152/tjg.2018.17330 · Cited by 397
The double edge sword of fibrosis in cancer
Chandler, C., Liu, T., Buckanovich, R. J., & Coffman, L. G. (2019) · Translational research · doi:10.1016/j.trsl.2019.02.006 · Cited by 257
Moghadasi, S., Elveny, M., Rahman, H. S., Suksatan, W., Jalil, A. T., Abdelbasset, W. K., Yumashev, A. V., Shariatzadeh, S., Motavalli, R., Behzad, F., et al. (2021) · Journal of Translational Medicine · doi:10.1186/s12967-021-02980-6 · Cited by 207
Retracted
Metadata
- Authors
- Zhang, C.-Y., Yuan, W.-G., He, P., Lei, J.-H., & Wang, C.-X.
- Affiliations
- Huazhong University of Science and Technology (CN)
- Venue
- World Journal of Gastroenterology
- Publisher
- Baishideng Publishing Group Inc.
- Published
- 2016
- Volume
- 22
- Issue
- 48
- Pages
- 10512
- ISSN
- 1007-9327 (ISSN-L)
- PMC
- PMC5192262
- OpenAlex
- W2565367159
- Cited by
- 594
- References
- 112
- Citations by year
- 2026: 37 · 2025: 70 · 2024: 75 · 2023: 80 · 2022: 84 · 2021: 88 · 2020: 60 · 2019: 59 · 2018: 24 · 2017: 15
- FWCI
- 4.07
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc
- Locations
- World Journal of Gastroenterology (publishedVersion, cc-by-nc)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (81300251)
- 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, hepatic stellate cells, liver cirrhosis, hepatocellular carcinoma, antifibrotic therapy, fibrogenic factors, collagen synthesis, myofibroblasts, viral hepatitis, schistosomiasis, alcoholic liver disease, cell-cell crosstalk, therapeutic target
- MeSH terms
- Resveratrol, Ursolic Acid, Acetyl-CoA C-Acetyltransferase, Animals, Fatty Liver, Alcoholic, Humans, Interleukins, Liver Cirrhosis, Macrophages, Schistosomiasis, Stilbenes, Triterpenes, Ursodeoxycholic Acid, Virus Diseases, Signal Transduction, CD4-Positive T-Lymphocytes, Disease Progression, MicroRNAs, Intracellular Signaling Peptides and Proteins, T-Lymphocytes, Regulatory, Hepatic Stellate Cells, Molecular Targeted Therapy, LIM Domain Proteins, Non-alcoholic Fatty Liver Disease
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