Pathological functions of hypoxia in endometriosis

Hsiao, Kuei‐Yang; Lin, Su-Shia; Wu, Ming‐Ho; Tsai, Shaw-Jenq

doi:10.2741/e736

Cited by 36 publications

(35 citation statements)

References 83 publications

(108 reference statements)

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“…According to Sampson's theory, when shed endometrial cells or debris retrogrades to the peritoneal cavity, the first stress faced is the local altered hypoxic microenvironment. A growing body of evidence suggests that peritoneal local hypoxia play an important role in endometriosis development and progression and the expression of hypoxia‐inducible factor‐1alpha (HIF‐1α) was increased significantly in the development of endometriosis …”

Section: Discussionmentioning

confidence: 99%

“…Hypoxia has a pathophysiological effect through the process of disease and regulation of gene expression . Numerous studies have suggested that peritoneal hypoxia is intricately involved in the pathogenesis of ovarian endometriosis . The key factor mediating cellular hypoxia response is the hypoxia‐inducible factor‐1 (HIF‐1), which is a heterodimeric transcription factor composed of an O 2 ‐sensitive α‐subunit and a constitutively expressed β‐subunit .…”

Section: Introductionmentioning

confidence: 99%

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Long non‐coding RNA MALAT1 mediates hypoxia‐induced pro‐survival autophagy of endometrial stromal cells in endometriosis

Liu

Zhang

Xiong

et al. 2018

J Cellular Molecular Medi

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Endometriosis is a common gynecological disease characterized by diminished apoptosis, sustained ectopic survival of dysfunctional endometrial cells. Hypoxia has been implicated as a crucial microenvironmental factor that contributes to endometriosis. It has been reported that long non‐coding RNA MALAT1 (lncRNA‐MALAT1) highly expressed in endometriosis and up‐regulated by hypoxia. Hypoxia may also induce autophagy, which might act as cell protective mechanism. However, the relationship between lncRNA‐MALAT1 and autophagy under hypoxia conditions in endometriosis remains unknown. In the present study, we found that both lncRNA‐MALAT1 and autophagy level were up‐regulated in ectopic endometrium from patients with endometriosis, and its expression level correlates positively with that of hypoxia‐inducible factor‐1α (HIF‐1α). In cultured human endometrial stromal cells, both lncRNA‐MALAT1 and autophagy were induced by hypoxia in a time‐dependent manner and lncRNA‐MALAT1 up‐regulation was dependent on HIF‐1α signalling. Our analyses also show that knockdown of lncRNA‐MALAT1 suppressed hypoxia induced autophagy. Furthermore, inhibiting autophagy with specific inhibitor 3‐Methyladenine (3‐MA) and Beclin1 siRNA enhanced apoptosis of human endometrial stromal cells under hypoxia condition. Collectively, our findings identify that lncRNA‐MALAT1 mediates hypoxia‐induced pro‐survival autophagy of endometrial stromal cells in endometriosis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Long non‐coding RNA MALAT1 mediates hypoxia‐induced pro‐survival autophagy of endometrial stromal cells in endometriosis

Liu

Zhang

Xiong

et al. 2018

J Cellular Molecular Medi

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“…Remarkably, hypoxic conditions alone can dramatically change the behavior of endometrial cells that are otherwise "normal", manifesting in increased estrogen production and other "abnormal" phenotypes [96]. More remarkably, activated platelets can activate HIF-1α in endometrial and endometriotic stromal cells, effectively generating a state of hypoxia [97].…”

Section: Revamping the Tiar Theory: The Endometrial-myometrial Interfmentioning

confidence: 99%

The Pathogenesis of Adenomyosis vis-à-vis Endometriosis

Guo

2020

JCM

104

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Adenomyosis is used to be called endometriosis interna, and deep endometriosis is now called adenomyosis externa. Thus, there is a question as to whether adenomyosis is simply endometriosis of the uterus, either from the perspective of pathogenesis or pathophysiology. In this manuscript, a comprehensive review was performed with a literature search using PubMed for all publications in English, related to adenomyosis and endometriosis, from inception to June 20, 2019. In addition, two prevailing theories, i.e., invagination-based on tissue injury and repair (TIAR) hypothesis-and metaplasia, on adenomyosis pathogenesis, are briefly overviewed and then critically scrutinized. Both theories have apparent limitations, i.e., difficulty in falsification, explaining existing data, and making useful predictions. Based on the current understanding of wound healing, a new hypothesis, called endometrial-myometrial interface disruption (EMID), is proposed to account for adenomyosis resulting from iatrogenic trauma to EMI. The EMID hypothesis not only highlights the more salient feature, i.e., hypoxia, at the wounding site, but also incorporates epithelial mesenchymal transition, recruitment of bone-marrow-derived stem cells, and enhanced survival and dissemination of endometrial cells dispersed and displaced due to iatrogenic procedures. More importantly, the EMID hypothesis predicts that the risk of adenomyosis can be reduced if certain perioperative interventions are performed. Consequently, from a pathogenic standpoint, adenomyosis is not simply endometriosis of the uterus, and, as such, may call for interventional procedures that are somewhat different from those for endometriosis to achieve the best results.

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“…2 Thus, in this review, the focus is on how it might be regulated and interact with other epigenetic elements. Hypoxia and inflammation, two critical driving forces for the development of endometriosis, 3,4 modulate the expression of DNMTs distinctly and can act together to cause aberrant DNA methylation patterns 1,5,6 (Figure 1). Two recent reports found that global methylation decreases in ectopic stromal cells, 1,6 which is mainly caused by hypoxia-mediated DNMT1 downregulation ( Figure 1, left).…”

Section: Alteration Of Dna Methylation In Endometriosismentioning

confidence: 99%

Epigenetic regulation of the pathological process in endometriosis

Hsiao

Tsai

2017

Reprod Medicine & Biology

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BackgroundEndometriosis is one of the most common gynecological diseases that greatly compromises the quality of life in affected individuals. A growing body of evidence shows that the remodeling of retrograde endometrial tissues to the ectopic endometriotic lesions involves multiple epigenetic alterations, such as DNA methylation, histone modification, and microRNA expression.MethodsThis article retrospectively reviewed the studies that were related to the epigenetic regulatory factors that contribute to the development and maintenance of endometriosis. A literature search was performed in order to collect scientific articles that were written in English by using the key words of “endometriosis,” “epigenetics,” “DNA methylation,” “histone modification,” and “microRNA.”ResultsEpigenetic modifications, including DNA methylation, histone modification, and microRNA expression, are involved in the pathogenesis of endometriosis. These epigenetic players are regulated or tuned by microenvironmental cues, such as locally produced estradiol, proinflammatory cytokines, and hypoxic stress, and reciprocally regulate the process or response to those stimuli.ConclusionUnderstanding the molecular mechanisms that underlie these epigenetic regulatory processes would shed light on the etiology and/or progression of endometriosis and facilitate the development of novel therapeutic strategies.

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Pathological functions of hypoxia in endometriosis

Cited by 36 publications

References 83 publications

Long non‐coding RNA MALAT1 mediates hypoxia‐induced pro‐survival autophagy of endometrial stromal cells in endometriosis

Long non‐coding RNA MALAT1 mediates hypoxia‐induced pro‐survival autophagy of endometrial stromal cells in endometriosis

The Pathogenesis of Adenomyosis vis-à-vis Endometriosis

Epigenetic regulation of the pathological process in endometriosis

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