Case-control study included 140 women with endometriosis and a control group consisting of 180 healthy fertile women without a history of endometriosis and/or autoimmune diseases from the ABC School of Medicine.
Since patients with endometriosis frequently use aspirin or other non-aspirin Non-Steroidal Anti-Inflammatory Drugs (NSAIDs), the aim of this study was to verify whether aspirin and other NSAIDs enhance MRP4 expression in 12Z human endometriotic epithelial cells and whether this was peroxisome proliferator-activated receptor alpha (PPARa) dependent.
We report for the first time that MRP4 is expressed in human endometrium, elevated in peritoneal endometriosis, and modulated by LXA(4) in endometriotic epithelial cells.
However, the ACC/ACC genotype showed a significant association because this genotype was significantly higher among patients with endometriosis than in healthy controls [OR = 3.55 (CI = 1.42–18.92); P = 0.006].
This study investigates whether angiotensin I-converting enzyme (ACE) *A2350G and A-240T gene polymorphisms could be used as markers of susceptibility in endometriosis.
This study investigates whether angiotensin I-converting enzyme (ACE) *A2350G and A-240T gene polymorphisms could be used as markers of susceptibility in endometriosis.
This review will focus on the signaling and effects of the potent chemokine CXCL12, and its long-known G protein-coupled receptor CXCR4, as well as the alternate receptor CXCR7 on the female reproductive tract and related diseases such as endometriosis, Asherman's syndrome, leiomyomas, endometrial cancer, and ovarian cancer.
In conclusion, overexpression of CXCR7 in different cellular populations of endometriosis microenvironment may play a role in the pathogenesis and represent a novel target for treatment.
These findings suggest that carriers of high activity ACP1 genotypes are more susceptible to endometriosis but less susceptible to allergic manifestations than carriers of other ACP1 genotypes.
These findings suggest that carriers of high activity ACP1 genotypes are more susceptible to endometriosis but less susceptible to allergic manifestations than carriers of other ACP1 genotypes.
We found that H19 and ACTA2 levels were significantly higher in endometriosis euESCs than in control euESCs (P < 0.05) and were positively correlated in endometriosis euESCs.
The hypothesis is based on the clinical and experimental observations that correlate the location of endometrial lesions with areas of mesothelial damage, together with genetic evidence that 4 genes associated with endometriosis are direct regulators of the actin-cytoskeleton, which coordinates mesothelial barrier integrity.
Focal adhesion, regulation of actin cytoskeleton, MAPK and TGFB/SMAD signaling pathway may be important molecular mechanism underlying the pathogenesis of endometriosis.
Btk inhibitor Ibrutinib prevented lesion growth, reduced mRNA expression of cyclooxygenase-2, alpha smooth muscle actin and type I collagen in the lesions and skewed activated B cells toward Bregs in the spleen and peritoneal cavity of mice with endometriosis.
The cytoskeletal proteins alpha-actinin, Ezrin, and talin are De-expressed in endometriosis and endometrioid carcinoma compared with normal uterine epithelium.