Vascular endothelial growth factor (VEGF) inhibition—a critical review
Abstract
Angiogenesis, or formation of new blood capillaries from preexisting vessels, plays both beneficial and damaging roles in the organism. It is a result of a complex balance of positive and negative regulators, and vascular endothelial growth factor (VEGF) is one of the most important pro-angiogenic factors involved in tumor angiogenesis. VEGF increases vascular permeability, which might facilitate tumor dissemination via the circulation causing a greater delivery of oxygen and nutrients; it recruits circulating endothelial precursor cells, and acts as a survival factor for immature tumor blood vessels. The endotheliotropic activities of VEGF are mediated through the VEGF-specific tyrosine-kinase receptors: VEGFR-1, VEGFR-2 and VEGFR-3. VEGF and its receptors play a central role in tumor angiogenesis, and therefore the blockade of this pathway is a promising therapeutic strategy for inhibiting angiogenesis and tumor growth. A number of different strategies to inhibit VEGF signal transduction are in development and they include the development of humanized neutralizing anti-VEGF monoclonal antibodies, receptor antagonists, soluble receptors, antagonistic VEGF mutants, and inhibitors of VEGF receptor function. These agents can be divided in two broad classes, namely agents designed to target the VEGF activity and agents designed to target the surface receptor function. The main purpose of this review is to summarize all the available information regarding the importance of the pro-angiogenic factor VEGF in cancer therapy. After an overview of the VEGF family and their respective receptors, we shall focus our attention on the different VEGF-inhibitors existent nowadays. Agents based upon anti-VEGF therapy have provided solid proofs about their success, and therefore we believe that a critical review is of the utmost importance to help researchers in their future work.
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In cancer, serum albumin concentration decreases, vascular permeability increases, absolute synthesis increases, half-life decreases, total mass decreases, distribution volume decreases, and VEGF increases.
“Cancer | ↓ to ↓↓ | ↑ to↑↑ | ↑ to↑↑ | ↓ to ↓↓ | ↓ to ↓↓ | ↓ to ↓↓ | ↑41, 42 | Anti‐VEGF beneficial in renal cancer but deleterious for kidney function”
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Macrophage heterogeneity in neovascularization
Jetten, N. (2014) · doi:10.26481/dis.20140509nj · Cited by 1 · see citing works
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- Authors
- Sousa Moreira, I., Alexandrino Fernandes, P., & Joao Ramos, M.
- Affiliations
- REQUIMTE/Departamento de Quimica, Faculdade de Ciencias da Universidade do Porto, Rua do Campo Alegre 687, 4169-007 Porto - Portugal., Portugal
- Venue
- Anti-Cancer Agents in Medicinal Chemistry
- Publisher
- Bentham Science Publishers Ltd.
- Published
- 2007-03-01
- Volume
- 7
- Issue
- 2
- Pages
- 223-245
- ISSN
- 1568-0118 (ISSN-L)
- 1871-5206
- OpenAlex
- W2144429930
- Cited by
- 110
- References
- 0
- Citations by year
- 2025: 4 · 2024: 2 · 2023: 2 · 2022: 7 · 2021: 3 · 2020: 2 · 2019: 5 · 2018: 4 · 2017: 9 · 2016: 10 · 2015: 9 · 2014: 5 · 2013: 9 · 2012: 5
- FWCI
- 3.95
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Anti-Cancer Agents in Medicinal Chemistry (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
- Health Sciences › Medicine › Oncology › Lymphatic System and Diseases
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cancer Mechanisms and Therapy
- Keywords
- vascular endothelial growth factor, VEGF inhibition, angiogenesis, tumor angiogenesis, VEGF receptors, VEGFR1, VEGFR2, VEGFR-3, anti-VEGF monoclonal antibody, VEGF receptor antagonist, soluble VEGF receptor, VEGF inhibitors, cancer therapy, VEGF family
- MeSH terms
- Animals, Humans, Models, Molecular, Neovascularization, Pathologic, Angiogenesis Inhibitors, Receptors, Vascular Endothelial Growth Factor, Vascular Endothelial Growth Factor A
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