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Cited by 277Liver Disease and TransplantationLiver physiology and pathologyLiver Disease Diagnosis and Treatment

The DOI matches its Crossref record; 189 of the 194 references it cites were found in a registry or an index.

Angiogenesis in chronic liver disease and its complications: Angiogenesis in CLD

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Coulon, Stephanie, Heindryckx, Femke, Geerts, Anja, Van Steenkiste, Christophe, Colle, Isabelle, Van Vlierberghe, Hans·2011·Liver International
DOI 10.1111/j.1478-3231.2010.02369.x
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Abstract

Nowadays, liver cancer, cirrhosis and other liver-related diseases are the fifth most common cause of mortality in the UK. Furthermore, chronic liver diseases (CLDs) are one of the major causes of death, which are still increasing year-on-year. Therefore, knowledge about the pathophysiology of CLDs and its complications is of uttermost importance. The goal of this review is to clarify the role of angiogenesis in the disease progression of various liver diseases. Looking closer at the pathophysiology of portal hypertension (PH), fibrosis, cirrhosis, non-alcoholic steatohepatitis (NASH) and hepatocellular carcinoma (HCC), we find that angiogenesis is a recurring factor in the disease progression. In PH, several factors involved in its pathogenesis, such as hypoxia, oxidative stress, inflammation and shear stress are potential mediators for the angiogenic response. The progression from fibrosis to cirrhosis, the end-point of CLDs, is distinguished by a prolonged inflammatory and fibrogenic process that leads to an abnormal angioarchitecture distinctive for cirrhosis. In several stages of NASH, a link might be made between the disease progression and hepatic microvasculature changes. HCC is one of the most vascular solid tumours in which angiogenesis plays an important role in its development, progression and metastasis. The close relationship between the progression of CLDs and angiogenesis emphasises the need for anti-angiogenic therapy as a tool for blocking or slowing down the disease progression. The fact that angiogenesis plays a pivotal role in CLDs gives rise to new opportunities for treating CLDs and its complications.

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Crossref · 10.1111/j.1478-3231.2010.02369.x

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189 of 189 references verified0 citation errors · 0 not checkable

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Research works printed but not linked: 2

  1. Ko, 2002, Nuclear factor kappaB dependency of platelet-activating factor-induced angiogenesis, Cancer Res, 62, 1809
  2. Cayon, 2008, Gene expression in obese patients with non-alcoholic steatohepatitis, Rev Esp Enferm Dig, 100, 212

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Metadata

Authors
Coulon, S., Heindryckx, F., Geerts, A., Van Steenkiste, C., Colle, I., & Van Vlierberghe, H.
Affiliations
Ghent University (BE)
ORCID
Venue
Liver International
Publisher
Wiley
Published
2010-11-15
Volume
31
Issue
2
Pages
146-162
ISSN
  • 0106-9543 (ISSN-L)
  • 1478-3223
DOI
10.1111/j.1478-3231.2010.02369.x
OpenAlex
W1484083850
Cited by
276
References
194
Citations by year
2026: 13 · 2025: 11 · 2024: 17 · 2023: 19 · 2022: 15 · 2021: 24 · 2020: 14 · 2019: 13 · 2018: 20 · 2017: 25 · 2016: 22 · 2015: 26 · 2014: 25 · 2013: 12 · 2012: 14
FWCI
1.40
Type
journal article
Language
en
Open access
Licence
doi.wiley.com/10.1002/tdm_license_1.1 (tdm, 1751 d)
Locations
  • Liver International (publishedVersion)
  • PubMed (publishedVersion)
  • Ghent University Academic Bibliography (Ghent University) (submittedVersion)
Topics
  • Health Sciences › Medicine › Hepatology › Liver Disease and Transplantation
  • Health Sciences › Medicine › Hepatology › Liver physiology and pathology
  • Health Sciences › Medicine › Hepatology › Liver Disease Diagnosis and Treatment
Keywords
angiogenesis, chronic liver disease, portal hypertension, liver fibrosis, liver cirrhosis, nonalcoholic steatohepatitis, hepatocellular carcinoma, hypoxia, oxidative stress, inflammation, shear stress, hepatic microvasculature, anti-angiogenic therapy, disease progression
MeSH terms
Chronic Disease, Fatty Liver, Fibroblast Growth Factors, Carcinoma, Hepatocellular, Humans, Hypertension, Portal, Liver Cirrhosis, Liver Neoplasms, Models, Biological, Neovascularization, Pathologic, Platelet-Derived Growth Factor, Signal Transduction, Cadherins, Integrins, Disease Progression, Thrombospondins, Angiogenesis Inhibitors, Receptors, Vascular Endothelial Growth Factor, Vascular Endothelial Growth Factor A, Angiopoietins, Angiostatins, Endostatins, Hypoxia-Inducible Factor 1, Microvessels, Non-alcoholic Fatty Liver Disease

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