{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,25]],"date-time":"2026-08-25T13:21:56Z","timestamp":1787664116272,"version":"build-2736575974"},"reference-count":31,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2026,8,11]],"date-time":"2026-08-11T00:00:00Z","timestamp":1786406400000},"content-version":"vor","delay-in-days":10,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"},{"start":{"date-parts":[[2026,8,1]],"date-time":"2026-08-01T00:00:00Z","timestamp":1785542400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82271684"],"award-info":[{"award-number":["82271684"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["American J Rep Immunol"],"published-print":{"date-parts":[[2026,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>Defective endometrial receptivity is an indispensable cause of infertility in endometriosis, yet the post\u2010transcriptional regulatory mechanisms underlying this impairment remain poorly understood. The goal of this research was to describe how miR\u201029c\u20103p and its target, COL4A1, regulate endometrial epithelial cell function and embryo adhesion.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Endometrial epithelial cells were obtained from 14 women (including 7 with endometriosis and 7 controls) undergoing in vitro fertilization (IVF). Expression levels of miR\u201029c\u20103p and COL4A1 were quantified. Gain\u2010 and loss\u2010of\u2010function tests were employed in Ishikawa cells to assess cell adhesion capabilities and delineate downstream signaling pathways implicated in implantation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Women with endometriosis had considerably higher levels of miR\u201029c\u20103p expression in their endometrial epithelium. Mechanistically, increased expression of miR\u201029c\u20103p suppressed COL4A1, downregulated E\u2010cadherin, and impaired JAr spheroid attachment. Notably, COL4A1 knockdown recapitulated these phenotypes by encouraging epithelial\u2010mesenchymal transition (EMT), thereby compromising adhesive capacity.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      Our findings identify the miR\u201029c\u20103p\/COL4A1\/\n                      <jats:italic>\u03b2<\/jats:italic>\n                      \u2010catenin axis as a pivotal hub controlling endometrial epithelial adhesion. In patients with endometriosis, this axis could be a potential molecular candidate to enhance fertility outcomes and restore endometrial receptivity.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/aji.70291","type":"journal-article","created":{"date-parts":[[2026,8,11]],"date-time":"2026-08-11T15:40:01Z","timestamp":1786462801000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["MiR\u201029c\u20103p Impairs the Adhesion of Endometrial Epithelial Cells via COL4A1\/\n                    <i>\u03b2<\/i>\n                    \u2010catenin in Endometriosis"],"prefix":"10.1111","volume":"96","author":[{"ORCID":"https:\/\/orcid.org\/0009-0002-1148-9289","authenticated-orcid":false,"given":"Chengyuan","family":"Li","sequence":"first","affiliation":[{"name":"Center For Reproductive Medicine Peking University Shenzhen Hospital Shenzhen China"},{"name":"Medical College Shantou University Medical College  Shantou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jian","family":"Li","sequence":"additional","affiliation":[{"name":"Center For Reproductive Medicine Peking University Shenzhen Hospital Shenzhen China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xin","family":"Li","sequence":"additional","affiliation":[{"name":"Center For Reproductive Medicine Peking University Shenzhen Hospital Shenzhen China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lan","family":"Geng","sequence":"additional","affiliation":[{"name":"Center For Reproductive Medicine Peking University Shenzhen Hospital Shenzhen China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qiuju","family":"Zhang","sequence":"additional","affiliation":[{"name":"Center For Reproductive Medicine Peking University Shenzhen Hospital Shenzhen China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhenhui","family":"Hou","sequence":"additional","affiliation":[{"name":"Center For Reproductive Medicine Peking University Shenzhen Hospital Shenzhen China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xi","family":"Xia","sequence":"additional","affiliation":[{"name":"Center For Reproductive Medicine Peking University Shenzhen Hospital Shenzhen China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,8,11]]},"reference":[{"key":"e_1_2_11_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0140\u20106736(21)00389\u20105"},{"key":"e_1_2_11_3_1","doi-asserted-by":"publisher","DOI":"10.1136\/bmj\u20102022\u2010070750"},{"key":"e_1_2_11_4_1","doi-asserted-by":"publisher","DOI":"10.3390\/biom13030430"},{"key":"e_1_2_11_5_1","doi-asserted-by":"publisher","DOI":"10.1093\/humrep\/deab123"},{"key":"e_1_2_11_6_1","doi-asserted-by":"publisher","DOI":"10.1093\/humrep\/deab032"},{"key":"e_1_2_11_7_1","doi-asserted-by":"publisher","DOI":"10.3892\/ijmm.2022.5179"},{"key":"e_1_2_11_8_1","doi-asserted-by":"publisher","DOI":"10.3390\/ijms23116210"},{"key":"e_1_2_11_9_1","doi-asserted-by":"publisher","DOI":"10.3390\/biomedicines12112618"},{"key":"e_1_2_11_10_1","doi-asserted-by":"publisher","DOI":"10.3390\/ijms241915001"},{"key":"e_1_2_11_11_1","doi-asserted-by":"publisher","DOI":"10.3892\/ijmm.2015.2082"},{"key":"e_1_2_11_12_1","first-page":"141","article-title":"Progesterone Resistance in Endometriosis Is Modulated by the Altered Expression of MicroRNA\u201029c and FKBP4","volume":"102","author":"Joshi N. 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