Cited by 595Liver physiology and pathologyLiver Disease Diagnosis and TreatmentLiver Disease and Transplantation

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Liver fibrosis and hepatic stellate cells: Etiology, pathological hallmarks and therapeutic targets

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Zhang, Chong-Yang, Yuan, Wei-Gang, He, Pei, Lei, Jia-Hui, Wang, Chun-Xu·2016·World Journal of Gastroenterology

DOI 10.3748/wjg.v22.i48.10512PMC PMC5192262

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Abstract

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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Figure 1 Initiation, progression, and resolution of liver fibrosis involving hepatic stellate cells. Upon various types of chronic injury - including that caused by alcohol, viral and schistosome infection, nonalcoholic steatohepatitis (NASH), and other factors - hepatic stellate cells (HSCs) transdifferentiate from quiescent HSCs to activated HSCs, the latter of which secrete abundant extracellular proteins that contribute to liver fibrosis. Liver fibrosis is thought to be a reversible condition owing to the elimination of causative agents and different strategies of limiting HSC activation; however, they cannot totally return to a quiescent status of the naive HSCs. Instead, they exhibit a pre-activated intermediate condition with an increased sensitivity to injury. Thus, preventing recurrent chronic liver injury is of great importance in patients undergoing treatment for liver fibrosis. Untreated or relapsed fibrosis progresses to liver cirrhosis, which often requires hepatic transplantation.CC BY-NC · PubMed Central

Figure 2 Roles of interleukin-30, hydrogen peroxide inducible clone 5, and cholesterol acyltransferase 1 in liver fibrosis.CC BY-NC · PubMed Central

Figure 3 Roles of the Wnt, TGF-β/Smad, and Gas6/Axl signaling pathways in the progression of liver fibrosis.CC BY-NC · PubMed Central

Figure 4 Mechanism of action of three potential therapeutic drugs-ursolic acid, 24-nor-ursodeoxycholic acid, and resveratrol-for treating fibrosis.CC BY-NC · PubMed Central

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Additional file 2 of miR-541 is associated with the prognosis of liver cirrhosis and directly targets JAG2 to inhibit the activation of hepatic stellate cells
Liu, J.-P., Song, S.-H., Shi, P.-M., Qin, X.-Y., Zheng, B.-N., Liu, S.-Q., Ding, C.-H., Zhang, X., Xie, W., Shi, Y.-H., et al. (2024) · Figshare · doi:10.6084/m9.figshare.25282931
Additional file 2 of Elastic modulus-reflected liver lesion stiffness relates to worse prognosis in pancreatic cancer patients with liver metastasis
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Additional file 1 of miR-541 is associated with the prognosis of liver cirrhosis and directly targets JAG2 to inhibit the activation of hepatic stellate cells
Liu, J.-P., Song, S.-H., Shi, P.-M., Qin, X.-Y., Zheng, B.-N., Liu, S.-Q., Ding, C.-H., Zhang, X., Xie, W., Shi, Y.-H., et al. (2024) · Figshare · doi:10.6084/m9.figshare.25282849
Additional file 2 of The effects of TGF-β-induced activation and starvation of vitamin A and palmitic acid on human stem cell-derived hepatic stellate cells
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Self-citation
Additional file 1 of The effects of TGF-β-induced activation and starvation of vitamin A and palmitic acid on human stem cell-derived hepatic stellate cells
Wilhelmsen, I., Combriat, T. M. D., Dalmao‐Fernández, A., Stokowiec, J., Wang, C., Olsen, P. A., Wik, J. A., Boichuk, Y., Aizenshtadt, A., & Krauss, S. J. K. (2024) · Figshare · doi:10.6084/m9.figshare.26360951
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Additional file 1 of Elastic modulus-reflected liver lesion stiffness relates to worse prognosis in pancreatic cancer patients with liver metastasis
Dong, S., Miao, X., Zhang, K., Zhu, X., Gao, Y., & Chen, H. (2023) · Figshare · doi:10.6084/m9.figshare.24030765
Additional file 3 of The effects of TGF-β-induced activation and starvation of vitamin A and palmitic acid on human stem cell-derived hepatic stellate cells
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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)
DOI: 10.3748/wjg.v22.i48.10512
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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Liver fibrosis and hepatic stellate cells: Etiology, pathological hallmarks and therapeutic targets

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