Pathogenesis of endometriosis: The role of genetics, inflammation and oxidative stress
2nd Department of Obstetrics and Gynecology, University of Athens, Athens, Greece. Archives of Gynecology
(Impact Factor: 1.36).
05/2012; 286(1):99-103. DOI: 10.1007/s00404-012-2357-8
Endometriosis is defined as the presence of endometrial tissue outside the uterine cavity.
The etiology of this multifactorial disease is still unresolved and an increasing number of studies suggest that genetic, hormonal, environmental, immunological and oxidative factors may all play an important role in the pathogenesis of this disorder.
In this literature review, inflammatory activity, oxidative stress as well as genetic abnormalities and mutations have been studied in an effort to identify factors predisposing to endometriosis.
Available from: Maria Grazia Porpora
- "Endometriosis is a gynecological condition characterized by the presence of ectopic endometrial tissue (endometrial glands and stroma) outside the uterus associated with pelvic pain and infertility . The disease affects 6-10% of women in reproductive age with or without pelvic pain and more than 30% of infertile women [2-4]. Endometriosis has a multifactorial inheritance: environmental pollutants, particularly dioxins and polychlorinated biphenyls (PCBs) and genetic predisposition have been suggested to concur to the onset and progression of this disease [5-8]. "
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The aim of this study was to determine whether the serotonin transporter gene (5-HTT), a key component in the control of the serotonergic system, is associated with endometriosis in an Italian population.
A case–control study, comprising 137 Italian patients with surgically confirmed endometriosis and 120 healthy controls, was carried out. 5-HTT genotypes (LL, SL and SS) were obtained by polymerase chain reaction and gel electrophoresis analysis. We found no overall difference in genotypic and allelic distributions of the 5-HTT gene between cases and controls.
Our results suggest that the 5-HTT L/S promoter polymorphism is not associated with susceptibility to endometriosis in the studied Italian patients.
Journal of Negative Results in BioMedicine 06/2014; 13(1):12. DOI:10.1186/1477-5751-13-12 · 1.47 Impact Factor
Available from: Pirdel Manizheh
- "free radical species in the Fenton reaction, leading to deregulation of cellular processes, cell dysfunction, and eventually to apoptosis or necrosis through lipid peroxidation, protein, and DNA damage (Papanikolaou & Pantopoulos 2005, Rahman et al. 2012). The presence of iron overload has been demonstrated in various components of the peritoneal cavity of endometriosis patients (peritoneal fluid, macrophages, and endometriotic lesions; Defrere et al. 2008, Augoulea et al. 2012), which strongly suggests disruption of iron homeostasis in the peritoneal cavity of patients. Iron overload in the peritoneal fluid provokes oxidative injury and inflammatory response, involving peritoneal macrophages in particular, which promote the proliferative capacity of ectopic implants of endometrium in the peritoneal cavity (Van Langendonckt et al. 2002b, Szczepariska et al. 2003). "
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ABSTRACT: This manuscript presents an overview of the involvement of iron overload-induced nitric oxide overproduction in apoptosis of peritoneal macrophages of women with endometriosis. We have postulated that the peritoneal iron overload is originated from retrograde menstruation or bleeding lesions in the ectopic endometrium, which may contribute to the development of endometriosis by a wide range of mechanisms, including oxidative damage and chronic inflammation. Excessive nitric oxide production may also be associated with impaired clearance of endometrial cells by macrophages, which promotes cell growth in the peritoneal cavity. Therefore, further research of the mechanisms and consequences of macrophage apoptosis in endometriosis help to discover novel therapeutic strategies which are designed to prevent progression of endometriosis.
Reproduction 03/2014; 147(6). DOI:10.1530/REP-13-0552 · 3.17 Impact Factor
Available from: Ann Aschengrau
- "Several factors may contribute to endometriosis development and disease severity, including anatomic (Breech and Laufer 1999), anthropometric (Missmer et al. 2004a), hormonal, immunologic (Siristatidis et al. 2006), inflammatory, and genetic factors (Augoulea et al. 2012; Nyholt et al. 2012). Inflammatory markers are elevated in women with endometriosis (Gentilini et al. 2011); a state of inflammation is considered both to be a result of the disease and to perhaps promote disease progression (Agic et al. 2006). "
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ABSTRACT: Particulate matter and proximity to large roadways may promote disease mechanisms, including systemic inflammation, hormonal alteration, and vascular proliferation, that may contribute to the development and severity of endometriosis.
To determine the association of air pollution exposures during adulthood, including distance to road, particulate matter less than 10 microns, less than 2.5 microns, and between 2.5 and 10 microns (PM2.5, PM10-2.5, PM10), and timing of exposure with risk of endometriosis in the Nurses' Health Study II.
Proximity to major roadways and outdoor levels of PM2.5, PM10-2.5, PM10 were determined for all residential addresses from 1993 to 2007. Multivariable-adjusted time-varying Cox proportional hazard models were used to estimate the relation between these air pollution exposures and endometriosis risk.
Among 84,060 women 2,486 incident cases of surgically confirmed endometriosis were identified over 710,230 person-years of follow-up. There was no evidence of an association, between distance to road, PM2.5, PM10-2.5, PM10 averaged over follow-up or during the previous 2- or 4- year period and endometriosis risk.
Traffic and air pollution exposures during adulthood were not associated with incident endometriosis in this cohort of women.
Environmental Health Perspectives 11/2013; 122(1). DOI:10.1289/ehp.1306627 · 7.98 Impact Factor
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