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Angiogenesis in chronic liver disease and its complications: Angiogenesis in CLD
Open accessAbstract
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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“Liver disease, Child A, B, or C | ↓ to ↓↓↓ | ↑ to↑↑↑ | ↓ to ↓↓↓ | ↑ !! | ↓ to ↓↓ | ↓ to ↓↓↓ | ↑165 | VEGF upregulated in cancer; anti‐VEGF treatment considered promising”
From Hypoalbuminemia: Pathogenesis and Clinical Significance (2019) · cites this paper as [165]
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Metadata
- Authors
- Coulon, S., Heindryckx, F., Geerts, A., Van Steenkiste, C., Colle, I., & Van Vlierberghe, H.
- Affiliations
- Ghent University (BE)
- Venue
- Liver International
- Publisher
- Wiley
- Published
- 2010-11-15
- Volume
- 31
- Issue
- 2
- Pages
- 146-162
- ISSN
- 0106-9543 (ISSN-L)
- 1478-3223
- 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
- bronze
- doi.org
- 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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