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. 2021 Jan 14;11:1345. doi: 10.1038/s41598-020-79750-9

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Illustrative diagram showing the possible intervention/therapeutic effects on endometriosis through the cholinergic anti-inflammatory pathway (CAIP). Endometriosis can induce pain and infertility, which can cause stress and depression, which, in turn, can lead to the activation of the HPA/SAM axes, resulting in increased release of catecholamines such as noradrenaline. The increased noradrenaline levels may induce the suppression of the DRD2 signaling pathway, the activation of the adrenergic receptor β2 (ADRB2), and the subsequent activation of the ADRB2/CREB/PKA signaling pathway, leading to increased angiogenesis and cellular proliferation, and thus lesional progression. Endometriotic lesions and inflammation are mutually stimulatory, and inflammation may also activate nociceptors such as TRPV1, facilitating pain sensation. The CAIP can be activated either by VNS or by α7nAChR agonists, leading to suppression, abrogation or attenuation of depression, pain, and inflammation, thereby achieving the therapeutic results.