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Updated: Aug 26, 2026
Noninvasive Monitoring of Lesion Size in a Heterologous Mouse Model of Endometriosis
Published on: February 26, 2019
Antiangiogenesis therapy for endometriosis
Annemiek W Nap1, Arjan W Griffioen, Gerard A J Dunselman
1Department of Obstetrics and Gynecology, Research Institute for Growth and Development, Maastricht University and University Hospital, 6202 AZ Maastricht, The Netherlands.
Abstract:
It is known that angiogenesis is of pivotal importance for the development of endometriosis. However, in the treatment of endometriosis patients, prevention of endometriosis lesion development only will not be sufficient as a therapy. Treatment options, aimed at interfering with established lesions, have to be developed. In this study we evaluated whether inhibition of angiogenesis by angiostatic therapy is also effective in antagonizing the sustentation of endometriosis. We evaluated the effect of the angiostatic compounds antihuman vascular endothelial growth factor, TNP-470, endostatin, and anginex on the growth of established endometriosis lesions in the nude mouse model. We show that human endometrium in the proliferative endometrium is highly angiogenic and that vascular endothelial growth factor-A is the most important angiogenesis promotory factor. The angiostatic compounds significantly decreased microvessel densities and the number of established endometriosis lesions. In the remaining lesions, the number of pericyte-protected vessels is not different in control and treated mice; however, the number of unprotected vessels was significantly reduced in the groups treated with the angiostatic agents. Our data demonstrate that inhibitors of angiogenesis effectively interfere with the maintenance and growth of endometriosis by inhibiting angiogenesis. This suggests that the use of angiostatic agents may be promising as a therapy for endometriosis.
Insights
Angiostatic therapy effectively targets established endometriosis lesions by inhibiting angiogenesis. This approach shows promise for treating endometriosis by reducing lesion growth and microvessel density.
Area of Science:
- Gynecology
- Oncology
- Vascular Biology
Background:
- Angiogenesis is crucial for endometriosis development.
- Current treatments focus on preventing lesion formation, but therapies targeting established lesions are needed.
- Inhibiting angiogenesis may offer a novel therapeutic strategy for endometriosis.
Purpose of the Study:
- To evaluate the efficacy of angiostatic therapy in treating established endometriosis lesions.
- To assess the impact of specific angiostatic compounds on endometriosis growth in a preclinical model.
Main Methods:
- Utilized a nude mouse model of endometriosis.
- Administered angiostatic compounds including anti-human vascular endothelial growth factor, TNP-470, endostatin, and anginex.
- Quantified microvessel density and lesion counts post-treatment.
Main Results:
- Human endometrium exhibits high angiogenic potential, driven by vascular endothelial growth factor-A.
- Angiostatic agents significantly reduced microvessel density and the number of established endometriosis lesions.
- Treatment led to a significant decrease in pericyte-unprotected vessels within remaining lesions.
Conclusions:
- Inhibitors of angiogenesis effectively impede the maintenance and growth of endometriosis.
- Angiostatic agents demonstrate therapeutic potential for endometriosis by targeting neovascularization.
- This study supports the development of angiostatic therapies for managing endometriosis.