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endometriosis/نقص الأكسجة
يتم حفظ الارتباط في الحافظة
الصفحة 1 من عند 79 النتائج
Estrogen stabilizes hypoxia-inducible factor 1α through G protein-coupled estrogen receptor 1 in eutopic endometrium of endometriosis.
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To investigate whether G protein-coupled estrogen receptor (GPER, also known as GPR30 and GPER1) stabilizes hypoxia-inducible factor 1α (HIF-1α) in eutopic endometrium (EuEM) of endometriosis.
Immunohistochemical analysis and experimental in vitro study.
University hospital.
Patients with or without
[Expression of hypoxia-inducible factor-1alpha in endometriosis].
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OBJECTIVE
To detect the expression of hypoxia-inducible factor-1alpha(HIF-1alpha) in endometriosis and explore the possible role of HIF-1alpha in the pathogenesis of endometriosis.
METHODS
Immunohistochemistry was performed to examine the expression of HIF-1alpha in 20 normal endometrium, 20 ectopic
Estrogen receptor expression affected by hypoxia inducible factor-1α in stromal cells from patients with endometriosis.
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OBJECTIVE
Endometriosis is an estrogen-dependent disease. The aim of this study was to evaluate the different expression of estrogen receptors (ER) and its relation to hypoxia inducible factor-1α (HIF-1α) in stromal cells from women with endometriosis.
METHODS
Paired eutopic endometrial and ectopic
Hypoxia Promotes Invasion of Endometrial Stromal Cells via Hypoxia-Inducible Factor 1α Upregulation-Mediated β-Catenin Activation in Endometriosis.
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Endometriosis is a common benign gynecological disease defined as the presence of endometrial tissue outside the uterine cavity. The aim of this study was to identify the molecular mechanism underlying hypoxia-induced increases in invasive ability of human endometrial stromal cells (HESCs). Herein,
Targeting hypoxia-mediated YAP1 nuclear translocation ameliorates pathogenesis of endometriosis without compromising maternal fertility.
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Endometriosis is a highly prevalent gynaecological disease that severely reduces women's health and quality of life. Ectopic endometriotic lesions have evolved mechanisms to survive in the hypoxic peritoneal microenvironment by regulating the expression of a significant subset of genes. However, the
Coordination of AUF1 and miR-148a destabilizes DNA methyltransferase 1 mRNA under hypoxia in endometriosis.
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OBJECTIVE
DNA methylation is regulated by hypoxia in endometriosis.
UNASSIGNED
Hypoxia causes global hypomethylation through AU-rich element binding factor 1 (AUF1)/microRNA-148a (miR-148a)-mediated destabilization of DNA methyltransferase 1 (DNMT1) mRNA.
BACKGROUND
Eutopic endometrial and ectopic
Hypoxia: The force of endometriosis.
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Hypoxia-inducible factor-1alpha: A promising therapeutic target in endometriosis.
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Endometriosis is a common gynecologic disease defined as the presence of ectopic endometrial tissues on the ovaries and pelvic peritoneum, and it is a significant cause of pelvic pain, dysmenorrhea and infertility of women in their reproductive age. However, the etiology of endometriosis remains
Pathological functions of hypoxia in endometriosis.
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Endometriosis is one of the most common gynecological diseases that significantly reduce the life quality of affected women. Research results from the past decade clearly demonstrated that aberrant production of estrogen and cyclooxygenase-2-derived prostaglandin E2 play indispensable roles in the
TET1 may contribute to hypoxia-induced epithelial to mesenchymal transition of endometrial epithelial cells in endometriosis
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Background: Endometriosis (EMs) is a non-malignant gynecological disease, whose pathogenesis remains to be clarified. Recent studies have found that hypoxia induces epithelial-mesenchymal transition (EMT) as well as epigenetic
Hypoxia, cytokines and stromal recruitment: parallels between pathophysiology of encapsulating peritoneal sclerosis, endometriosis and peritoneal metastasis.
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Peritoneal response to various kinds of injury involves loss of peritoneal mesothelial cells (PMC), danger signalling, epithelial-mesenchymal transition and mesothelial-mesenchymal transition (MMT). Encapsulating peritoneal sclerosis (EPS), endometriosis (EM) and peritoneal metastasis (PM) are all
Hypoxia Promotes Ectopic Adhesion Ability of Endometrial Stromal Cells via TGF-β1/Smad Signaling in Endometriosis.
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Hypoxia plays a vital role in the progression of endometriosis. Additionally, integrin-mediated aberrant adhesion is also essential for establishment of endometriotic lesions. In this study, we sought to determine the function of hypoxia in integrin-mediated adhesion of endometrial stromal cells
Hypoxia-inducible factor 1α-induced epithelial-mesenchymal transition of endometrial epithelial cells may contribute to the development of endometriosis.
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How does hypoxia promote growth of lesions in the development of endometriosis?
Hypoxia induces the epithelial-mesenchymal transition (EMT) of endometrial cells, resulting in changes in cellular characteristics, which may be a prerequisite for the establishment of endometriotic lesions.
Up-regulated
Autophagy contributes to hypoxia-induced epithelial to mesenchymal transition of endometrial epithelial cells in endometriosis.
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Endometriosis is a benign gynecologic disorder, it presents with malignant characteristics, such as migration and invasion. Hypoxia has been implicated in triggering epithelial-mesenchymal transition (EMT). Hypoxia is also known to induce autophagy. However, the relationship between autophagy and
Inhibition of dual specificity phosphatase-2 by hypoxia promotes interleukin-8-mediated angiogenesis in endometriosis.
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OBJECTIVE
How does hypoxia-mediated down-regulation of dual specificity phosphatase-2 (DUSP2) promote endometriotic lesion development?
CONCLUSIONS
Inhibition of DUSP2 by hypoxia enhances endometriotic lesion growth via promoting interleukin-8 (IL-8)-dependent angiogenesis.
BACKGROUND
Angiogenesis
قاعدة بيانات الأعشاب الطبية الأكثر اكتمالا التي يدعمها العلم
- يعمل في 55 لغة
- العلاجات العشبية مدعومة بالعلم
- التعرف على الأعشاب بالصورة
- خريطة GPS تفاعلية - ضع علامة على الأعشاب في الموقع (قريبًا)
- اقرأ المنشورات العلمية المتعلقة ببحثك
- البحث عن الأعشاب الطبية من آثارها
- نظّم اهتماماتك وابقَ على اطلاع دائم بأبحاث الأخبار والتجارب السريرية وبراءات الاختراع
اكتب أحد الأعراض أو المرض واقرأ عن الأعشاب التي قد تساعد ، واكتب عشبًا واطلع على الأمراض والأعراض التي تستخدم ضدها.
* تستند جميع المعلومات إلى البحوث العلمية المنشورة
