{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T14:11:33Z","timestamp":1792159893815,"version":"4.4.0"},"reference-count":38,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2023,8,29]],"date-time":"2023-08-29T00:00:00Z","timestamp":1693267200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Acad Dermatol Venereol"],"published-print":{"date-parts":[[2023,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Rosacea is a common chronic inflammatory skin condition that is often refractory to treatment, with frequent relapses. Alterations in the skin immunological response and\n                      <jats:italic>Demodex<\/jats:italic>\n                      mite infestation are the primary aetiologic factors targeted for treatment. Transient receptor potential cation channel subfamily V member 1 (TRPV1) is a nociceptive cation channel that plays a role in cutaneous neurogenic pain and can be activated by various rosacea triggers.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>\n                      We investigated the effects of TRPV1 modulation in rosacea, focussing on\n                      <jats:italic>Demodex<\/jats:italic>\n                      mite colonization and cutaneous neurogenic inflammation.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We examined mRNA expression levels according to\n                      <jats:italic>Demodex<\/jats:italic>\n                      population counts. An in vitro study using capsazepine as a TRPV1 antagonist was performed to assess the influence of TRPV1 in keratinocytes. A rosacea\u2010like mouse model was generated by the injection of the 37\u2010amino acid C\u2010terminal cathelicidin peptide (LL37), and changes in the skin, dorsal root ganglion (DRG) and ears were examined.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Increased\n                      <jats:italic>Demodex<\/jats:italic>\n                      mite population counts were associated with increased expression levels of TRPV1, tropomyosin receptor kinase A (TrkA) and nerve growth factor (NGF), and these levels could be reduced by capsazepine treatment in keratinocytes. In an in vivo study, the downstream effects of TRPV1 activation were investigated in the skin, DRG and ears of the rosacea\u2010like mouse model.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>The findings of this study are instrumental for understanding the underlying causes of rosacea and could potentially lead to the development of new treatments targeting the NGF\u2013TrkA\u2013TRPV1 pathway. The identification of this pathway as a therapeutic target could represent a major breakthrough for rosacea research, potentially resulting in more effective and targeted rosacea treatments. This study contributes to an improved understanding of rosacea pathophysiology, which may lead to the development of more effective treatments in the future.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/jdv.19449","type":"journal-article","created":{"date-parts":[[2023,8,22]],"date-time":"2023-08-22T10:40:08Z","timestamp":1692700808000},"page":"2589-2600","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":29,"title":["Cutaneous neurogenic inflammation mediated by\n                    <scp>TRPV1<\/scp>\n                    \u2013\n                    <scp>NGF<\/scp>\n                    \u2013\n                    <scp>TRKA<\/scp>\n                    pathway activation in rosacea is exacerbated by the presence of\n                    <i>Demodex<\/i>\n                    mites"],"prefix":"10.1111","volume":"37","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6237-9031","authenticated-orcid":false,"given":"Sang Gyu","family":"Lee","sequence":"first","affiliation":[{"name":"Department of Dermatology &amp; Cutaneous Biology Research Institute Yonsei University College of Medicine  Seoul South Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0047-5941","authenticated-orcid":false,"given":"Jihee","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Dermatology, Yongin Severance Hospital Yonsei University College of Medicine  Yongin South Korea"},{"name":"Scar Laser and Plastic Surgery Center Yonsei Cancer Hospital  Seoul South Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6831-7379","authenticated-orcid":false,"given":"Young In","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Dermatology &amp; Cutaneous Biology Research Institute Yonsei University College of Medicine  Seoul South Korea"},{"name":"Scar Laser and Plastic Surgery Center 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