The DOI matches its Crossref record; 231 of the 231 references it cites were found in a registry or an index.
Angiogenesis: regulators and clinical applications
Abstract
Angiogenesis is a fundamental process in reproduction and wound healing. Under these conditions, neovascularization is tightly regulated. Unregulated angiogenesis may lead to several angiogenic diseases and is thought to be indispensable for solid tumor growth and metastasis. The construction of a vascular network requires different sequential steps including the release of proteases from "activated" endothelial cells with subsequent degradation of the basement membrane surrounding the existing vessel, migration of endothelial cells into the interstitial space, endothelial cell proliferation, and differentiation into mature blood vessels. These processes are mediated by a wide range of angiogenic inducers, including growth factors, chemokines, angiogenic enzymes, endothelial specific receptors, and adhesion molecules. Finally, when sufficient neovascularization has occurred, angiogenic factors are down-regulated or the local concentration of inhibitors increases. As a result, the endothelial cells become quiescent, and the vessels remain or regress if no longer needed. Thus, angiogenesis requires many interactions that must be tightly regulated in a spatial and temporal manner. Each of these processes presents possible targets for therapeutic intervention. Synthetic inhibitors of cell invasion (marimastat, Neovastat, AG-3340), adhesion (Vitaxin), or proliferation (TNP-470, thalidomide, Combretastatin A-4), or compounds that interfere with angiogenic growth factors (interferon-alpha, suramin, and analogues) or their receptors (SU6668, SU5416), as well as endogenous inhibitors of angiogenesis (endostatin, interleukin-12) are being evaluated in clinical trials against a variety of solid tumors. As basic knowledge about the control of angiogenesis and its role in tumor growth and metastasis increases, it may be possible in the future to develop specific anti-angiogenic agents that offer a potential therapy for cancer and angiogenic diseases.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“VEGF levels are known to be regulated by hypoxia, insulin stimulation, certain growth factors, and specific cytokines (79)”
From Adipose tissue remodeling and obesity (2011) · cites this paper as [79]
Citations
Cites
Angiogenesis in cancer, vascular, rheumatoid and other disease
Folkman, J. (1995) · Nature Medicine · doi:10.1038/nm0195-27 · Cited by 7,627
The tumour suppressor protein VHL targets hypoxia-inducible factors for oxygen-dependent proteolysis
Maxwell, P. H., Wiesener, M. S., Chang, G.-W., Clifford, S. C., Vaux, E. C., Cockman, M. E., Wykoff, C. C., Pugh, C. W., Maher, E. R., & Ratcliffe, P. J. (1999) · Nature · doi:10.1038/20459 · Cited by 5,180
Endostatin: an endogenous inhibitor of angiogenesis and tumor growth
O'Reilly, M. S., Boehm, T., Shing, Y., Fukai, N., Vasios, G., Lane, W. S., Flynn, E., Birkhead, J. R., Olsen, B. R., & Folkman, J. (1997) · Cell · doi:10.1016/s0092-8674(00)81848-6 · Cited by 4,486
Failure of blood-island formation and vasculogenesis in Flk-1-deficient mice
Shalaby, F., Rossant, J., Yamaguchi, T. P., Gertsenstein, M., Wu, X.-F., Breitman, M. L., & Schuh, A. C. (1995) · Nature · doi:10.1038/376062a0 · Cited by 3,931
Heterozygous embryonic lethality induced by targeted inactivation of the VEGF gene
Ferrara, N., Carver-Moore, K., Chen, H., Dowd, M., Lu, L., O’Shea, K. S., Powell-Braxton, L., Hillan, K. J., & Moore, M. W. (1996) · Nature · doi:10.1038/380439a0 · Cited by 3,661
Angiopoietin-2, a Natural Antagonist for Tie2 That Disrupts in vivo Angiogenesis
Maisonpierre, P. C., Suri, C., Jones, P. F., Bartunkova, S., Wiegand, S. J., Radziejewski, C., Compton, D., McClain, J., Aldrich, T. H., Papadopoulos, N., et al. (1997) · Science · doi:10.1126/science.277.5322.55 · Cited by 3,570
OʼReilly, M. (1994) · Cell · doi:10.1016/0092-8674(94)90200-3 · Cited by 3,344
Dvorak, H. F., Brown, L. F., Detmar, M. J., & Dvořàk, A. M. (1995) · Europe PMC (PubMed Central) · Cited by 3,100
Requisite Role of Angiopoietin-1, a Ligand for the TIE2 Receptor, during Embryonic Angiogenesis
Suri, C., Jones, P. F., Patan, S., Bartunkova, S., Maisonpierre, P. C., Davis, S. H., Sato, T. N., & Yancopoulos, G. D. (1996) · Cell · doi:10.1016/s0092-8674(00)81813-9 · Cited by 2,872
Folkman, J., & Shing, Y. (1992) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(19)49853-0 · Cited by 2,651
Research works printed but not linked: 6
- Moore, 1998, CXC chemokine modulation of angiogenesis, J Investig Med, 46, 113
- Montesano, 1992, Modulation of angiogenesisin vitro, EXS, 61, 129
- Liekens, 1999, A novel animal model for hemangiomas, Cancer Res, 59, 2376
- Tozer, 1999, Combretastatin A-4 phosphate as a tumor vascular-targeting agent, Cancer Res, 59, 1626
- Im, 1999, Antiangiogenesis treatment for gliomas, Cancer Res, 59, 895
- Kumar, 1999, Breast carcinoma, Cancer Res, 59, 856
Cited by
Sorted by citations
Adipose tissue remodeling and obesity
Sun, K., Kusminski, C. M., & Scherer, P. E. (2011) · Journal of Clinical Investigation · doi:10.1172/jci45887 · Cited by 1,941
Nitric oxide and wound repair: role of cytokines?
Schwentker, A., Vodovotz, Y., Weller, R., & Billiar, T. R. (2002) · Nitric Oxide · doi:10.1016/s1089-8603(02)00002-2 · Cited by 386
Bora, P. S., Sohn, J.-H., Cruz, J. M. C., Jha, P., Nishihori, H., Wang, Y., Kaliappan, S., Kaplan, H. J., & Bora, N. S. (2005) · The Journal of Immunology · doi:10.4049/jimmunol.174.1.491 · Cited by 249
Endothelial nitric oxide (NO) and its pathophysiologic regulation
Chatterjee, A., & Catravas, J. D. (2008) · Vascular Pharmacology · doi:10.1016/j.vph.2008.06.008 · Cited by 236
Kang, Y., Kim, J., Park, J., Lee, Y. M., Saravanakumar, G., Park, K. M., Choi, W., Kim, K., Lee, E., Kim, C., et al. (2019) · Biomaterials · doi:10.1016/j.biomaterials.2019.119297 · Cited by 108
Elimination of Neoangiogenesis for Plaque Stabilization
Kolodgie, F. D., Narula, J., Yuan, C., Burke, A. P., Finn, A. V., & Virmani, R. (2007) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2006.10.083 · Cited by 96
Regulation and Function of Matrix Metalloproteinase-13 in Cancer Progression and Metastasis
Li, S., Pritchard, D. M., & Yu, L.-G. (2022) · Cancers · doi:10.3390/cancers14133263 · Cited by 82
Metadata
- Authors
- Liekens, S., De Clercq, E., & Neyts, J.
- Affiliations
- Rega Institute for Medical Research (BE)
- Corresponding author
- Liekens, Sandra
- Venue
- Biochemical Pharmacology
- Publisher
- Elsevier BV
- Published
- 2001-02
- Volume
- 61
- Issue
- 3
- Pages
- 253-270
- ISSN
- 0006-2952 (ISSN-L)
- OpenAlex
- W2109197670
- Cited by
- 748
- References
- 231
- Citations by year
- 2026: 5 · 2025: 10 · 2024: 11 · 2023: 14 · 2022: 16 · 2021: 22 · 2020: 20 · 2019: 16 · 2018: 17 · 2017: 25 · 2016: 33 · 2015: 39 · 2014: 44 · 2013: 30 · 2012: 28
- FWCI
- 16.00
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Biochemical Pharmacology (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 › Oncology › Vascular Tumors and Angiosarcomas
- Keywords
- angiogenesis, neovascularization, angiogenesis inhibitors, anti-angiogenic therapy, tumor growth, metastasis, angiogenic factors, endothelial cell migration, basement membrane degradation, endostatin, marimastat, combretastatin A-4, thalidomide, wound healing, reproduction
- MeSH terms
- Humans, Neoplasms, Neovascularization, Pathologic, Neovascularization, Physiologic, Angiogenesis Inhibitors, Angiogenesis Inducing Agents
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
