{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T03:08:18Z","timestamp":1790564898301,"version":"4.1.0"},"reference-count":86,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2025,5,11]],"date-time":"2025-05-11T00:00:00Z","timestamp":1746921600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2025,5,11]],"date-time":"2025-05-11T00:00:00Z","timestamp":1746921600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2026,6]]},"abstract":"<jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>\n                      Gestational diabetes mellitus (GDM) is linked to altered fetal development and an increased risk of offspring developing cardiometabolic diseases in adulthood. The mechanisms responsible are unclear; however, GDM is associated with altered fetoplacental vascularisation, fibrosis and endothelial dysfunction. In non\u2010pregnant individuals with diabetes, similar vascular changes are attributed to disruptions in endothelial\u2010to\u2010mesenchymal transition (EndMT), a key process where endothelial cells adopt a mesenchymal phenotype. Here, we assess whether alterations in the fetoplacental macro\u2010 and microvasculature are attributed to EndMT, using human umbilical vein endothelial cells (HUVECs) and human term placental tissue, respectively. Transforming growth factor (TGF)\u2010\u03b22 and interleukin (IL)\u20101\u03b2 induced morphological and molecular changes consistent with EndMT in both GDM and non\u2010GDM HUVECs. The ability of TGF\u2010\u03b22 and IL\u20101\u03b2 to alter expression of known EndMT regulators,\n                      <jats:italic>VWF<\/jats:italic>\n                      ,\n                      <jats:italic>TGFBR1<\/jats:italic>\n                      ,\n                      <jats:italic>IL1B<\/jats:italic>\n                      and\n                      <jats:italic>IL1R1<\/jats:italic>\n                      , was diminished in GDM HUVECs; however, all other hallmarks of EndMT were similar. In placental villous tissue, Slug and Snail, two key transcriptional regulators of EndMT, were detected in the villous stroma, suggesting that EndMT probably occurs in the placental microvasculature. We observed a reduction in endothelial marker genes\n                      <jats:italic>PECAM1<\/jats:italic>\n                      ,\n                      <jats:italic>VWF<\/jats:italic>\n                      and\n                      <jats:italic>CDH5<\/jats:italic>\n                      in GDM placentas, suggesting reduced placental vascularisation. This was accompanied by a reduction in EndMT regulators\n                      <jats:italic>SNAI2<\/jats:italic>\n                      ,\n                      <jats:italic>TGB2<\/jats:italic>\n                      ,\n                      <jats:italic>TGFB3<\/jats:italic>\n                      and\n                      <jats:italic>TGFBR2<\/jats:italic>\n                      ; however, there was no change in mesenchymal markers or other EndMT regulators. This suggests that there may be some alterations in EndMT in GDM but this probably does not fully explain the endothelial dysfunction and altered vascularisation that occurs in the fetoplacental vasculature in pregnancies complicated by GDM.\n                      <jats:boxed-text content-type=\"graphic\" position=\"anchor\">\n                        <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/tjp16667-gra-0001-m.png\">\n                          <jats:alt-text>image<\/jats:alt-text>\n                        <\/jats:graphic>\n                      <\/jats:boxed-text>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>Gestational diabetes mellitus (GDM) has been linked to altered placental vascularisation, fibrosis and endothelial dysfunction.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Disruptions in endothelial\u2010to\u2010mesenchymal transition (EndMT), a process where endothelial cells adopt a mesenchymal phenotype, has been linked to vascular complications in diabetes, but EndMT in GDM has not been investigated.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>\n                            Transforming growth factor (TGF)\u2010\u03b22 and interleukin (IL)\u20101\u03b2 induced morphological and molecular changes consistent with EndMT in GDM and non\u2010GDM human umbilical vein endothelial cells (HUVECs). Although the expression of EndMT mediators,\n                            <jats:italic>VWF<\/jats:italic>\n                            ,\n                            <jats:italic>TGFBR1<\/jats:italic>\n                            ,\n                            <jats:italic>IL1B<\/jats:italic>\n                            , and\n                            <jats:italic>IL1R1<\/jats:italic>\n                            , was diminished in GDM HUVECs, other EndMT hallmarks were similar.\n                          <\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>\n                            Transcriptional regulators of EndMT, Slug and Snail, were detected in the human term placenta. Despite a reduction in endothelial markers,\n                            <jats:italic>PECAM1<\/jats:italic>\n                            ,\n                            <jats:italic>VWF<\/jats:italic>\n                            and\n                            <jats:italic>CDH5<\/jats:italic>\n                            , as well as\n                            <jats:italic>SNAI2<\/jats:italic>\n                            ,\n                            <jats:italic>TGFB2\/3<\/jats:italic>\n                            and\n                            <jats:italic>TGFBR2<\/jats:italic>\n                            in GDM placenta, there was no change in mesenchymal or other EndMT markers.\n                          <\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>This suggests that, although there may be some changes to EndMT in GDM, the vascular dysfunction is probably not explained fully by alterations in EndMT.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1113\/jp287931","type":"journal-article","created":{"date-parts":[[2025,5,11]],"date-time":"2025-05-11T11:43:18Z","timestamp":1746963798000},"page":"4405-4425","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Endothelial\u2010to\u2010mesenchymal transition in the fetoplacental macrovasculature and microvasculature in pregnancies complicated by gestational diabetes"],"prefix":"10.1113","volume":"604","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3936-2688","authenticated-orcid":false,"given":"Abigail R.","family":"Byford","sequence":"first","affiliation":[{"name":"Discovery and Translational Science Department, Leeds Institute of Cardiovascular and Metabolic Medicine, Faculty of Medicine and Health University of Leeds  Leeds 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