Possible involvement of neuropeptide and neurotransmitter receptors in Adenomyosis
Adenomyotic lesions showed increased NK1R, CRLR, RAMP1, and ADRB2 receptor expression and decreased α7nAChR expression compared to control endometrium.
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The study compared adenomyotic tissue from 30 women with adenomyosis to age- and menstrual-phase–matched control endometrial tissue from 24 women without adenomyosis, using immunohistochemistry to measure receptor immunoreactivity for neuropeptide/neurotransmitter pathways (RAMP1/CRLR for CGRP, NK1R for substance P, ADRB2 for noradrenaline) and α7 nicotinic acetylcholine receptor (α7nAChR), with fibrosis assessed by Masson trichrome staining and symptom data including dysmenorrhea. Staining levels of NK1R, CRLR, RAMP1, and ADRB2 were significantly elevated in adenomyotic lesions, while α7nAChR staining was significantly reduced, and dysmenorrhea severity correlated positively with lesional ADRB2 levels. The authors interpret these patterns as consistent with SP, CGRP, and noradrenaline promoting adenomyosis and acetylcholine potentially counteracting it, with a proposed feed-forward loop involving pain and lesion progression via ADRB2/HPA-SAM axes. A key limitation is that the work is based on receptor immunohistochemistry and correlations, without direct functional assays or mechanistic validation. This paper is centrally about adenomyosis—identifying altered expression of neuropeptide/neurotransmitter receptors in adenomyotic lesions that parallels known mechanisms in endometriosis.
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- Perioperative Suppression of Schwann Cell Dedifferentiation Reduces the Risk of Adenomyosis Resulting from Endometrial-Myometrial Interface Disruption in Mice 2022
- Higher Risk of Anxiety and Depression in Women with Adenomyosis as Compared with Those with Uterine Leiomyoma 2022
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