Abstract
Endometriosis, results in infertility in 50% infertile women. Explanations given are poor oocyte quality as well as low grade embryos associated with abnormal folliculogenesis, with reduced chances of fertilization correlated with enhanced oxidative stress, high reactive oxygen species (ROS) levels/local inflammation. Particularly escalated amounts of cytokines are found in follicular fluid of follicles of Endometriosis subjects. Here we further detail on the work going on in finding the role of granulosa cells in Endometriosis subjects with regards to increased inflammation, alteration in cytokines in follicular fluid that associates with follicular fluid in causing the oxidative stress, and how the upstream pathway involving tumour necrosis factor alpha (TNFα) and nuclear factor kappa B( NFκB) that influences both telomere length as well as telomerase activity, with shorter telomeres as well as reduced telomerase activity associated with aging follicles as well as those observed in patients with premature ovarian insufficiency (POI). Thus, this enhanced granulosa cell NFκB corresponds with inflammation found in FF along with effect on telomeres. Ways of targeting it seems to be one answer in improving reproductive potential of Endometriosis patients.
Highlights
Endometriosis, results in infertility in 50% infertile women [1]
Explanations given are poor oocyte quality as well as low grade embryos associated with abnormal folliculogenesis [2], with reduced chances of fertilization correlated with enhanced oxidative stress, high reactive oxygen species (ROS) levels/local inflammation [3]
Synthesis of anti-oxidant enzymes like peroxiredoxin 4, superoxide dismutase and catalase and oxidative stress damage response proteins like aldehyde dehydrogenase 3, member A2 reduces with aging in human granulosa lutein cells, that helps in an unbalance in ROS/anti-oxidants which modulate molecular injury as well as changes in cellular functioning .Increased oxidative stress in the granulosa cells associates with reduced expression of follicular stimulating hormone( FSH) receptor (FSHR) as well as a dysregulated FSHR signalling pathway and might have a role in impaired steroidogenic function as well as bad ovarian response to FSH in women who are aging
Summary
Endometriosis, results in infertility in 50% infertile women [1]. Explanations given are poor oocyte quality as well as low grade embryos associated with abnormal folliculogenesis [2], with reduced chances of fertilization correlated with enhanced oxidative stress, high reactive oxygen species (ROS) levels/local inflammation [3]. The antral follicle count (AFC), luteinizing hormone (LH) amounts as well as the number of oocytes recovered, and mature oocytes all were < in their Endometriomas group Stimulated by these observations they tried to evaluate the molecular reasons behind this effect on follicle formation via a number of repeated in vitro studies where they separated granulosa cell from the follicular fluid ,evaluated them for any basal inflammatory changes as well as culturing them in the exogenous inflammatory stimulants added for getting a response. Their observations were shorter telomeres but the granulosa cell telomerase activity (GTA) was same in PCOS subjects as compared to controls [19,20] In this study, they found that GTA in ovarian endometriotic subjects associated positively with the number of mature oocytes, negatively with granulosa cell NFκB activity and reduced following TNFα therapy. There is requirement for experiments detailing pathophysiology of granulosa cell in endometriotic subjects and time to unveil why subfertility in this disease both for patients as well as professionals [21]
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