Endometriosis and infertility: biomarkers affecting implantation rate

Carvalho, L.; Hui, Celene Yy; Agarwal, Ashok

doi:10.1586/17474108.2013.825456

Cited by 5 publications

(2 citation statements)

References 76 publications

(82 reference statements)

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“…At the molecular level, changes reflected in gene expression, proteome, and secretome occur. In particular, two robustly secreted molecules are the hallmark of decidualization: insulin-like growth factor binding protein-1 (IGFBP-1) and prolactin (PRL) (140), whose expression is related to PR activity (141,142). Both IGFBP-1 and PRL are drastically downregulated in the eutopic endometrium of women affected by endometriosis (143).…”

Section: Association Of Inflammation With Infertility In Patients Witmentioning

confidence: 99%

Regulation of Inflammation Pathways and Inflammasome by Sex Steroid Hormones in Endometriosis

et al. 2020

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Endometriosis is a gynecological disorder characterized by the growth of endometrial tissue (glands and stroma) outside the uterus, mainly in the peritoneal cavity, ovaries, and intestines. This condition shows estrogen dependency and progesterone resistance, and it has been associated with chronic inflammation, severe pain, and infertility, which negatively affect the quality of life in reproductive women. The molecular mechanisms involved in the pathogenesis of endometriosis are not completely understood; however, inflammation plays a key role in the pathophysiology of the disease, mainly by altering the function of immune cells (macrophages, natural killer, and T cells) and increasing levels of pro-inflammatory mediators in the peritoneal cavity, endometrium, and blood. These immune alterations inhibit apoptotic pathways and promote adhesion and proliferation of endometriotic cells, as well as angiogenesis and neurogenesis in endometriotic lesions. It has been demonstrated that hormonal alterations in endometriosis are related to the inflammatory unbalance in this disease. Particularly, steroid hormones (mainly estradiol) promote the expression and release of pro-inflammatory factors. Excessive inflammation in endometriosis contributes to changes of hormonal regulation by modulating sex steroid receptors expression and increasing aromatase activity. In addition, dysregulation of the inflammasome pathway, mediated by an alteration of cellular responses to steroid hormones, participates in disease progression through preventing cell death, promoting adhesion, invasion, and cell proliferation. Furthermore, inflammation is involved in endometriosis-associated infertility, which alters endometrium receptivity by impairing biochemical responses and decidualization. The purpose of this review is to present current research about the role of inflammasome in the pathogenesis of endometriosis as well as the molecular role of sex hormones in the inflammatory responses in endometriosis.

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Section: Association Of Inflammation With Infertility In Patients Witmentioning

confidence: 99%

Regulation of Inflammation Pathways and Inflammasome by Sex Steroid Hormones in Endometriosis

et al. 2020

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“…Endometrial receptivity is related to integrin expression of the endometrium; however, women with endometriosis have reduced expression of αvβ3, possibly due to decreased HOXA10 [ 93 ]. Other implantation-related biomarkers such as glycodelin A, osteopontin, LIF, lysophosphatidic acid receptor 3, and insulin-like growth factor binding protein 1 (IGFBP1) are also affected [ 94 ]. Expression of empty spiracles homolog 2 (EMX2) was elevated during the implantation window in endometriosis patients and associated with implantation failure [ 95 ].…”

Section: Chronic Niche Inflammation In Endometriosis Developmentmentioning

confidence: 99%

Chronic Niche Inflammation in Endometriosis-Associated Infertility: Current Understanding and Future Therapeutic Strategies

Lin

Chen

Chang

et al. 2018

IJMS

136

104

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Endometriosis is an estrogen-dependent inflammatory disease that affects up to 10% of women of reproductive age and accounts for up to 50% of female infertility cases. It has been highly associated with poorer outcomes of assisted reproductive technology (ART), including decreased oocyte retrieval, lower implantation, and pregnancy rates. A better understanding of the pathogenesis of endometriosis-associated infertility is crucial for improving infertility treatment outcomes. Current theories regarding how endometriosis reduces fertility include anatomical distortion, ovulatory dysfunction, and niche inflammation-associated peritoneal or implantation defects. This review will survey the latest evidence on the role of inflammatory niche in the peritoneal cavity, ovaries, and uterus of endometriosis patients. Nonhormone treatment strategies that target these inflammation processes are also included. Furthermore, mesenchymal stem cell-based therapies are highlighted for potential endometriosis treatment because of their immunomodulatory effects and tropism toward inflamed lesion foci. Potential applications of stem cell therapy in treatment of endometriosis-associated infertility in particular for safety and efficacy are discussed.

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Exosomal microRNAs and long noncoding RNAs: as novel biomarkers for endometriosis

et al. 2023

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Endometriosis and infertility: biomarkers affecting implantation rate

Cited by 5 publications

References 76 publications

Regulation of Inflammation Pathways and Inflammasome by Sex Steroid Hormones in Endometriosis

Regulation of Inflammation Pathways and Inflammasome by Sex Steroid Hormones in Endometriosis

Chronic Niche Inflammation in Endometriosis-Associated Infertility: Current Understanding and Future Therapeutic Strategies

Exosomal microRNAs and long noncoding RNAs: as novel biomarkers for endometriosis

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