{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T09:55:06Z","timestamp":1791453306456,"version":"4.3.3"},"reference-count":40,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T00:00:00Z","timestamp":1791417600000},"content-version":"vor","delay-in-days":280,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,1,1]],"date-time":"2026-01-01T00:00:00Z","timestamp":1767225600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100021171","name":"Basic and Applied Basic Research Foundation of Guangdong Province","doi-asserted-by":"publisher","award":["2022A1515110976"],"award-info":[{"award-number":["2022A1515110976"]}],"id":[{"id":"10.13039\/501100021171","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cardiovascular Therapeutics"],"published-print":{"date-parts":[[2026,1]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Endothelial\u2010to\u2010mesenchymal transition (EndMT) contributes to myocardial fibrosis after cardiac injury. Circular RNAs (circRNAs) have been implicated in the regulation of EndMT, but whether circRNAs participate in this process through translational potential remains unclear. This study investigated the role of circIdh2 in EndMT and examined whether its coding capacity may contribute to its biological effects.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Rat endothelial progenitor cells (rEPCs) were treated with TGF\u2010\n                      <jats:italic>\u03b2<\/jats:italic>\n                      1 (5\u2009ng\/mL) for 7 days to induce EndMT. The expression of circSorbs1, circIdh2, and circSntb2 was measured by qRT\u2010PCR. EndMT\u2010related markers, including VE\u2010cadherin, vimentin, and N\u2010cadherin, were detected by western blotting. Cell migration was assessed using Transwell and scratch wound healing assays. The translational potential of circIdh2 was examined using an Idh2\u2010IRES luciferase reporter assay, FLAG immunoprecipitation followed by western blotting, and mass spectrometry. A circIdh2 mutant construct and a rat model of acute myocardial infarction (AMI) were used to further evaluate the contribution of circIdh2 and its putative circIdh2\u2010derived product.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      TGF\u2010\n                      <jats:italic>\u03b2<\/jats:italic>\n                      1 reduced the expression of circSorbs1, circIdh2, and circSntb2 in rEPCs. CircIdh2 showed the largest decrease in the initial qRT\u2010PCR screen and was selected before any circIdh2\u2010specific functional experiment. The Idh2 host gene supplied metabolic and redox context for the prespecified screen but was not used as evidence of circIdh2 function. CircIdh2 overexpression increased VE\u2010cadherin expression, decreased vimentin and N\u2010cadherin expression, and attenuated TGF\u2010\n                      <jats:italic>\u03b2<\/jats:italic>\n                      1\u2013induced cell migration. In contrast, circIdh2 knockdown promoted EndMT\u2010associated marker changes and cell migration. The Idh2\u2010IRES reporter assay, FLAG immunoprecipitation, and mass spectrometry supported the translational potential of circIdh2 and detected a FLAG\u2010tagged product derived from the circIdh2 expression construct. The FLAG\u2010tagged circIdh2 expression construct modulated EndMT\u2010related markers and reduced cell migration, whereas the coding\u2010disrupted mutant construct did not reproduce the effects of wild\u2010type circIdh2. In vivo, AAV\u2010mediated delivery of circIdh2 or circIdh2\u2010aa attenuated myocardial fibrosis and partly reversed EndMT\u2010related marker changes after AMI.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>CircIdh2 attenuated EndMT\u2010associated changes in rEPCs and was associated with reduced myocardial fibrosis after AMI. These findings support the translational potential of circIdh2 and suggest that its putative circIdh2\u2010derived product may contribute to its effects.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1155\/cdr\/2005876","type":"journal-article","created":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T09:38:14Z","timestamp":1791452294000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["CircIdh2 Attenuates Endothelial\u2010to\u2010Mesenchymal Transition and Myocardial Fibrosis and Exhibits Translational Potential"],"prefix":"10.1155","volume":"2026","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2271-3349","authenticated-orcid":false,"given":"Yanjia","family":"Chen","sequence":"first","affiliation":[{"name":"Department of Anesthesiology Southern Medical University Nanfang Hospital  Guangzhou China  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