Endometrial angiogenesis

In: Angiogenesis · 1998 · vol. 2(4) , pp. 287–294 · doi:10.1023/a:1009222030539 · PMID:14517449 · W4234379883
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This review examines endometrial angiogenesis timing and mechanisms, identifying VEGF as a key factor, but notes unclear timing and limited inhibitor studies, hindering full understanding.

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This paper reviews how endometrial angiogenesis is timed during the menstrual cycle, the mechanisms thought to form endometrial capillaries, and the angiogenesis factors and inhibitors identified in endometrium. It synthesizes endothelial cell proliferation data and concludes that the timing of angiogenesis across the cycle remains unclear, with capillary formation likely involving elongation and intussusception rather than sprouting. The review highlights many angiogenic factors, especially VEGF, but states that there is no evidence linking expression of a specific factor to the actual occurrence of angiogenesis, and only limited work addresses inhibitors despite the presence of potential inhibitor precursors. Relevance to endometriosis: the paper cites prior work on VEGF steroid regulation and mentions endometriosis in the context of studies localizing growth factors (e.g., fibroblast growth factor) in endometrium of women with endometriosis, though the paper’s main focus is endometrial angiogenesis in physiology.

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Abstract

As a tissue that exhibits rapid cyclical growth and shedding throughout the reproductive life of the female, the human endometrium provides a good model for the study of normal physiological angiogenesis. This paper will review current information on the timing of angiogenesis during the menstrual cycle, the mechanisms involved in endometrial capillary formation, and current information on angiogenesis factors and inhibitors. Based on endothelial cell proliferation studies, the timing of angiogenesis during the menstrual cycle remains unclear. The major mechanism by which endometrial capillaries are formed is probably a mixture of elongation and intussusception, with minimal evidence currently available for sprouting. Numerous angiogenesis factors have been identified in endometrium, the most well studied of which is VEGF. However, to date there is no evidence supporting a relationship between the expression of any given angiogenic factor and the occurrence of angiogenesis in the endometrium. Very limited studies have been undertaken to date on endometrial angiogenesis inhibitors, although the precursors to many of the known proteolytic fragments which act as inhibitors exist in the endometrium. In conclusion, neither the timing of vascular growth during the menstrual cycle nor the mechanisms by which endometrial vessels are formed are currently understood, thus placing major limitations on our understanding of how angiogenesis promoters and inhibitors may act in human endometrium.
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Abstract

As a tissue that exhibits rapid cyclical growth and shedding throughout the reproductive life of the female, the human endometrium provides a good model for the study of normal physiological angiogenesis. This paper will review current information on the timing of angiogenesis during the menstrual cycle, the mechanisms involved in endometrial capillary formation, and current information on angiogenesis factors and inhibitors. Based on endothelial cell proliferation studies, the timing of angiogenesis during the menstrual cycle remains unclear. The major mechanism by which endometrial capillaries are formed is probably a mixture of elongation and intussusception, with minimal evidence currently available for sprouting. Numerous angiogenesis factors have been identified in endometrium, the most well studied of which is VEGF. However, to date there is no evidence supporting a relationship between the expression of any given angiogenic factor and the occurrence of angiogenesis in the endometrium. Very limited studies have been undertaken to date on endometrial angiogenesis inhibitors, although the precursors to many of the known proteolytic fragments which act as inhibitors exist in the endometrium. In conclusion, neither the timing of vascular growth during the menstrual cycle nor the mechanisms by which endometrial vessels are formed are currently understood, thus placing major limitations on our understanding of how angiogenesis promoters and inhibitors may act in human endometrium. Similar content being viewed by others

References

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