2013
Endometriosis: hormone regulation and clinical consequences of chemotaxis and apoptosis
Abstract: Estrogens and progestogens modulate chemotaxis and apoptosis in human endometrium and endometriotic cells and tissues. These endocrine and paracrine pathways are perturbed in women with endometriosis, contributing to inflammatory responses, abnormal tissue remodeling, therapeutic refractoriness and disease persistence. Ultimately, they promote adhesion formation and the clinical symptoms of pelvic pain and infertility. A more detailed understanding of the molecular mechanisms involved will offer new opportunit…
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Cited by 272 publications
(226 citation statements)
References 141 publications
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“…A distribution of COX2 in endometriotic lesions (Ota et al, 2001) and increased COX2 mRNA expression in a mix of endometriotic lesions (Bukulmez et al, 2008) also supported an augmented prostaglandin secretion in these tissues. As PLA2G2A also induces vascular endothelial cell migration (Rizzo et al, 2000), our data support the link between inflammation and angiogenesis in endometriosis (Reis et al, 2013).…”
Section: Discussionsupporting
confidence: 73%
“…A distribution of COX2 in endometriotic lesions (Ota et al, 2001) and increased COX2 mRNA expression in a mix of endometriotic lesions (Bukulmez et al, 2008) also supported an augmented prostaglandin secretion in these tissues. As PLA2G2A also induces vascular endothelial cell migration (Rizzo et al, 2000), our data support the link between inflammation and angiogenesis in endometriosis (Reis et al, 2013).…”
Section: Discussionsupporting
confidence: 73%
“…Moreover, PCNA immunostaining appeared to be decreased in KO/KO mice and WT/WT mice treated with ISO-1. These data further support MIF pro-survival effects, its possible involvement in endometriotic cell resistance to apoptosis and its relevance to endometriosis as numerous alterations in the apoptotic pathways were detected in women with endometriosis, including a significant BCL2/BAX disequilibrium favoring the BCL2 survival pathway [54] – [56] .…”
Section: Discussionsupporting
confidence: 68%
“…This perspective provides a coherent explanation for the marked heterogeneity observed among patients, including differences in age at onset, anatomical distribution of lesions, symptom severity, and risk of recurrence. It also supports the concept that endometriosis is not a static condition but a continuously evolving disorder, in which biological, environmental, and temporal factors converge to define individual disease phenotypes [ 109 , 110 , 111 , 112 ].…”
Section: A Systemic Disease Model Of Endometriosissupporting
confidence: 71%
