Hormonal therapy potentiates the effect of surgery on gene expression profile of peripheral blood mononuclear cells in patients affected by endometriosis

Vignali, Michele; Pisoni, Serena; Gentilini, Davide; Spada, Elena; Solima, Eugenio; Viganò, Paola; Candiani, Massimo; Busacca, Mauro; Blasio, Anna Maria Di

doi:10.23736/s2724-6507.20.03298-8

Cited by 1 publication

(1 citation statement)

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“…As a natural response of innate and adaptive immune system components to try to eliminate menstrual debris, immune cell infiltration and resultant tissue repair are initiated. However, the inability to deal with the persistent presence of menstrual debris over time may lead to an immune system overload and subsequent immune alterations [10,11]. The activational actions of sex steroid hormones that have well-known modulatory effects on the immune responses of young women may predispose to immune-related disorders [12].…”

Section: Endometriosis As a Chronic Inflammatory Diseasementioning

confidence: 99%

Genetics and Inflammation in Endometriosis: Improving Knowledge for Development of New Pharmacological Strategies

Giacomini

Minetto

Piani

et al. 2021

IJMS

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According to a rich body of literature, immune cell dysfunctions, both locally and systemically, and an inflammatory environment characterize all forms of endometriosis. Alterations in transcripts and proteins involved in the recruitment of immune cells, in the interaction between cytokines and their receptors, cellular adhesion and apoptosis have been demonstrated in endometriotic lesions. The objective of this narrative review is to provide an overview of the components and mechanisms at the intersection between inflammation and genetics that may constitute vanguard therapeutic approaches in endometriosis. The GWAS technology and pathway-based analysis highlighted the role of the MAPK and the WNT/β-catenin cascades in the pathogenesis of endometriosis. These signaling pathways have been suggested to interfere with the disease establishment via several mechanisms, including apoptosis, migration and angiogenesis. Extracellular vesicle-associated molecules may be not only interesting to explain some aspects of endometriosis progression, but they may also serve as therapeutic regimens per se. Immune/inflammatory dysfunctions have always represented attractive therapeutic targets in endometriosis. These would be even more interesting if genetic evidence supported the involvement of functional pathways at the basis of these alterations. Targeting these dysfunctions through next-generation inhibitors can constitute a therapeutic alternative for endometriosis.

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Section: Endometriosis As a Chronic Inflammatory Diseasementioning

confidence: 99%