Villainous role of estrogen in macrophage-nerve interaction in endometriosis

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17β-estradiol 4 endocrinologydiseasesdrugs
raloxifene 4 endocrinologydiseasesdrugs
testosterone 1 endocrinologydiseasesdrugs

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17β-estradiol 8485 ERα and ERβ are significantly overexpressed in macrophages of endometriosis [[28]]. Treatment with 17β-estradiol in human macrophages in vitro induces an increase of ERα expression in macrophages. Furthermore, the
17β-estradiol 14793 cavity is confirmed to polarize macrophages from M1 toward M2 phenotype via CCL2/CCR pathway [[55]]. 17β-estradiol and TCDD (2, 3, 7, 8-tetrachlorodibenzo-p-dioxin) also have a synergistic effect on inducing M2 macrophages
17β-estradiol 17920 salivary gland [[65]]. It has been demonstrated that macrophages are one of the important sources of NGF. 17β-estradiol can induce c-Fos expression and shift the composition of NGF promoter, AP-1 from c-Jun homodimers to
17β-estradiol 26423 modulate corneal sensitivity by up-regulation of SP [[89]].The release of CGRP is also regulated by 17β-estradiol in the visceral pain sensitivity, implicating the role of estrogen in regulating of inflammatory neuropeptides
raloxifene 30590 activity at the ER. It is providing new treatment strategies for endometriosis [[98]]. Administration of raloxifene is effective in the treatment of chronic pelvic pain in women with endometriosis [[97]]. The mechanism
raloxifene 30707 effective in the treatment of chronic pelvic pain in women with endometriosis [[97]]. The mechanism of raloxifene action relies on its anti-inflammatory properties, exemplified by a decrease in M1 monocytes, macrophage
raloxifene 30992 IL-1β and IL-6 production [[99]]. A study has shown that there is an earlier return of pelvic pain in raloxifene group compared to the placebo group, hindering further development of raloxifene [[100]]. For recurrence
raloxifene 31073 of pelvic pain in raloxifene group compared to the placebo group, hindering further development of raloxifene [[100]]. For recurrence of chronic pain, accurate targeting of the ER in macrophages and nerve fibers
testosterone 29853 suppression of ovulation [[95]]. Danazol is widely used and promotes endometrial atrophy by increasing free testosterone levels leading to a hypoestrogenic state [[96]]. A recent study developed two ER ligands, chloroindazole
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