{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,23]],"date-time":"2026-08-23T16:06:27Z","timestamp":1787501187367,"version":"build-2736575974"},"reference-count":83,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2020,9,9]],"date-time":"2020-09-09T00:00:00Z","timestamp":1599609600000},"content-version":"vor","delay-in-days":8,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["STE 2312\/1\u20103"],"award-info":[{"award-number":["STE 2312\/1\u20103"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Experimental Dermatology"],"published-print":{"date-parts":[[2020,9]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Nicotinic acetylcholine receptors (nAChRs) are members of the superfamily of neurotransmitter\u2010gated ion channels. The natural ligand for nAChRs is the endogenous neurotransmitter acetylcholine. Among the nAChRs is the \u03b17nAChR. It is not only expressed by neural tissues but also in the skin. A number of different resident cutaneous cell types including epidermal keratinocytes, sebocytes and dermal fibroblasts express functional \u03b17nAChR. Moreover, cells of the immune system such as lymphocytes, macrophages and monocytes, playing an important role in skin homeostasis, also express \u03b17nAChR. Translational research focusing on the exploitation of the \u03b17nAChR in dermatology has revealed that this neuroendocrine receptor could be promising target for the treatment of inflammatory skin diseases. For example, \u03b17nAChR agonists can counteract transforming growth factor\u2010\u03b21\u2010mediated responses in dermal fibroblasts, key effector cells in scleroderma. In accordance with this \u03b17nAChR, agonists are effective in both inflammation and non\u2010inflammation\u2010driven models of experimentally induced skin fibrosis. Moreover, \u03b17nAChR agonists can modulate expression of proinflammatory cytokines in epidermal keratinocytes that are crucially involved in the pathogenesis of psoriasis and other inflammatory skin diseases. Finally, the capability of \u03b17nAChR agonists to suppress ultraviolet light A\/B\u2010induced responses, for example production of proinflammatory cytokines and oxidative stress, the latter crucially involved in dermal photoageing, points to a potential of such agents in the prevention of extrinsic skin ageing. Therefore, emphasis on translational research targeting the \u03b17nAChR in skin may lead to the development of new treatment and prevention modalities against fibrosclerotic skin diseases, psoriasis vulgaris, atopic dermatitis, acne, photodermatoses and extrinsic skin ageing.<\/jats:p>","DOI":"10.1111\/exd.14173","type":"journal-article","created":{"date-parts":[[2020,8,11]],"date-time":"2020-08-11T22:55:42Z","timestamp":1597186542000},"page":"924-931","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":35,"title":["Targeting the \u03b17 nicotinic acetylcholine receptor\u2013A novel road towards the future treatment of skin diseases"],"prefix":"10.1111","volume":"29","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5583-1950","authenticated-orcid":false,"given":"Agatha","family":"Stegemann","sequence":"first","affiliation":[{"name":"Dept. of Dermatology University of M\u00fcnster Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7338-7734","authenticated-orcid":false,"given":"Markus","family":"B\u00f6hm","sequence":"additional","affiliation":[{"name":"Dept. of Dermatology University of M\u00fcnster Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2020,9,9]]},"reference":[{"key":"e_1_2_8_2_1","first-page":"53","volume":"152","author":"Steinbach J. 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