Pathogenesis of endometriosis: Interaction between Endocrine and inflammatory pathways

Patel, Brijesh; Lenk, Emily E.; Lebovic, Dan I.; Shu, Yaqing; Yu, Jie; Taylor, Robert N.

doi:10.1016/j.bpobgyn.2018.01.006

Cited by 137 publications

(103 citation statements)

References 91 publications

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“…Inflammation is the main molecular and cellular process involved in the pathophysiology of endometriosis, causing pain, tissue remodeling, lesion formation, fibrosis, and infertility (6). Aberrant production and secretion of immune mediators like cytokines, prostaglandins, and metalloproteinases, as well as alteration of activity and infiltration of immune cells in sites of lesion and peritoneal cavity are some changes involved in this disrupted response (3,53).…”

Section: Alteration Of Inflammatory Functions In Endometriosismentioning

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: Alteration Of Inflammatory Functions In Endometriosismentioning

confidence: 99%

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

et al. 2020

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“…1,38,42 Endometriosis has an estimated prevalence of 5%-10% among women of reproductive age, rising to 30%-50% in patients with infertility and/or pain. 38 Initial studies showed that human endometrial stromal cells produce the chemokine CXCL12 and that bone marrow cells express the CXCL12 receptor, CXCR4. 38 Initial studies showed that human endometrial stromal cells produce the chemokine CXCL12 and that bone marrow cells express the CXCL12 receptor, CXCR4.…”

Section: Xcl12 S I G Naling In Endome Trios Ismentioning

confidence: 99%

“…Endometriosis is a common gynecologic disorder characterized by the presence of hormonally responsive ectopic implants of endometrial epithelium and stroma dispersed in extrauterine locations. 37 Although the etiology is not fully characterized, endometriosis is a multifactorial disorder, resulting from retrograde menstruation, 38 ectopic differentiation of stem cells, 39 dysregulation of immune/inflammatory cells, 40,41 and abnormal hormonal response. 1,38,42 Endometriosis has an estimated prevalence of 5%-10% among women of reproductive age, rising to 30%-50% in patients with infertility and/or pain.…”

Section: Xcl12 S I G Naling In Endome Trios Ismentioning

confidence: 99%

“…37 Although the etiology is not fully characterized, endometriosis is a multifactorial disorder, resulting from retrograde menstruation, 38 ectopic differentiation of stem cells, 39 dysregulation of immune/inflammatory cells, 40,41 and abnormal hormonal response. 1,38,42 Endometriosis has an estimated prevalence of 5%-10% among women of reproductive age, rising to 30%-50% in patients with infertility and/or pain. [43][44][45][46][47] Despite this estimated prevalence of disease, the etiology of endometriosis remains poorly understood.…”

Section: Xcl12 S I G Naling In Endome Trios Ismentioning

confidence: 99%

“…[43][44][45][46][47] Despite this estimated prevalence of disease, the etiology of endometriosis remains poorly understood. 38 Initial studies showed that human endometrial stromal cells produce the chemokine CXCL12 and that bone marrow cells express the CXCL12 receptor, CXCR4. 48 However, the interaction between CXCL12 and CXCR7 on BMDSC attraction and disease progression remains to be determined.…”

Section: Xcl12 S I G Naling In Endome Trios Ismentioning

confidence: 99%

See 2 more Smart Citations

The CXL12/CXCR4/CXCR7 axis in female reproductive tract disease: Review

Krikun

2018

American J Rep Immunol

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Initial studies on the chemokine stromal derived factor 1 (now referred to as CXCL12) were proposed to be enhanced in several diseases including those which affect the female reproductive tract. These include endometriosis, Asherman's syndrome, endometrial cancers, and ovarian cancers. Additionally, recent studies from our laboratory suggest that CXCL12 signaling is involved in leiomyomas (fibroids). These diseases present an inflammatory/hypoxic environment which further promotes pathology. At first, studies focused on signaling by CXCL12 via its well-known receptor, CXCR4. However, the discovery of CXCR7 as another receptor for CXCL12 with rather high binding affinity and recent reports about its involvement in endometrial disease and cancer progression has questioned the potential of "selective blockade"' of CXCR4 to treat these ailments. This review will focus on the signaling and effects of the potent chemokine CXCL12, and its long-known G protein-coupled receptor CXCR4, as well as the alternate receptor CXCR7 on the female reproductive tract and related diseases such as endometriosis, Asherman's syndrome, leiomyomas, endometrial cancer, and ovarian cancer. Although several other mechanisms are inherent to these diseases such as gene mutations, differential expression of miRNAs and epigenetics, for this review, we will focus on the CXCL12/CXCR4/CXCR7 axis as a novel target.

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The Basic Science of Endometriosis

Yong¹

2020

Female Sexual Pain Disorders

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Pathogenesis of endometriosis: Interaction between Endocrine and inflammatory pathways

Cited by 137 publications

References 91 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

The CXL12/CXCR4/CXCR7 axis in female reproductive tract disease: Review

The Basic Science of Endometriosis

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