Endometriosis
Surgery is more effective than medicinal intervention for addressing infertility associated with endometriosis. Surgery attempts to remove endometrial tissue and preserve the ovaries without damaging normal tissue. In-vitro fertilization (IVF) procedures are effective in improving fertility in many women with endometriosis.
VEZT
Endometriosis is a gynaecological disorder affecting 1 in 10 women in their reproductive years globally. This disorder occurs when endometrial tissue which grows inside the lining of the uterus grows on the outer surface of the uterus. The predominant symptoms of this are pelvic pain and infertility, however 25% of women who are inflicted with the disease may show none of these symptoms. Whilst the disease is usually non-fatal, it can have prolonged social and psychological effects on women and thus degrades their quality of life. Whilst the causes of the disease are still unclear, a certain number of genes have been linked to being a contributing factor for the disease. Of these, mutations in the VEZT gene have been identified by various Genome-wide association studies (GWAS). The VEZT gene is a complex gene, however it is known that the single nucleotide polymorphism (SNP) rs10859871 at locus 12q22 has been highly linked to being a genetic cause of endometriosis in women. An SNP is simply a variation that occurs in a single nucleotide in a specific region of a gene. Vezatin, the protein encoded by the VEZT gene is seen abundantly in endometrial and myometrial tissue, with localisation of the protein being both cytoplasmic and nuclear. This result was concurrent with previous literature stating the prominent role of vezatin in the regulation and maintenance of adherens junctions. This specific SNP is proven to cause an increase in vezatin expression within the endometrial cells, thus posing as a risk factor in the pathogenesis of endometriosis. Vezatin expression is also greater in ectopic endometrium as opposed to eutopic. Furthermore, vezatin expression is significantly increased in glandular endometrium during the secretory phase of the menstrual cycle. This result in conjunction with the finding that other adherens junction components also increase expression suggests that this process may be occurring in response to fluctuating progesterone levels. However, the mechanism of increased vezatin expression leading to the formation of ectopic endometrial tissues is unknown. Furthermore, there is much more scientific study required to directly link mutations in the VEZT gene to a direct cause of endometriosis.