The non-human primate model of endometriosis: research and implications for fecundity

Abstract

The development of an animal model of endometriosis is crucial for the investigation of disease pathogenesis and therapeutic intervention. These models will enhance our ability to evaluate the causes for the subfertility associated with disease and provide a first-line validation of treatment modulators. Currently rodents and non-human primate models have been developed, but each model has their limitations. The aim of this manuscript is to summarize the current findings and theories on the development of endometriosis and disease progression and the effectiveness of therapeutic targets using the experimental induced model of endometriosis in the baboon (Papio anubis).

Figure 1

Gene dysregulation in ectopic and eutopic endometrium in baboons and women with endometriosis. All references can be found within the manuscript. Red denotes upregulated genes, blue denotes downregulated genes. Abbreviations: TNF, tumour necrosis factor; TGF, transforming growth factor; ICAM, intracellular adhesion molecule; IL, interleukin; MMP, matrix metalloproteinase; VEGF, vascular endothelial growth factor; ESR, oestrogen receptor; PGR, progesterone receptor; HSD, hydroxysteroid dehydrogenase; LIF, leukaemia inhibitory factor; FKBP, regulator of progesterone responsiveness; IGFBP, insulin-like binding protein; CYR, cysteine-rich angiogenic inducer; Hic-5, progesterone responsive gene; avb3, integrin avb3.