{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,5]],"date-time":"2026-06-05T13:09:37Z","timestamp":1780664977570,"version":"3.54.1"},"reference-count":37,"publisher":"Scientific Scholar","content-domain":{"domain":["cytojournal.com"],"crossmark-restriction":true},"short-container-title":["Cytojournal"],"abstract":"<jats:sec id=\"st1\">\n                    <jats:title>Objectives:<\/jats:title>\n                    <jats:p>Myocardial infarction (MI) is linked to high mortality, which highlights the need for early diagnosis and intervention to prevent heart failure. N6-methyladenosine (m6A) methylation of ribonucleic acid (RNA) influences endothelial dysfunction and MI. Here, the effects and associated mechanisms of fat mass and obesity-associated gene (FTO) on vascular endothelial cell (EC) function, as well as myocardial damage in mice following MI were investigated.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"st2\">\n                    <jats:title>Material and Methods:<\/jats:title>\n                    <jats:p>A human umbilical vein EC (HUVEC) model of oxygen-glucose deprivation (OGD) as well as a mouse MI model were used to detect MI-induced endothelial and myocardial damage. EC function was examined using cell-counting-kit-8, wound healing, migration, and tube formation assays. Methylated RNA immunoprecipitation (MeRIP) sequencing and RNA sequencing were utilized to analyze the m6A modifications and RNA expression patterns in control and FTO-overexpressing ECs following OGD. FTO and ATP-binding cassette subfamily F member 1 (ABCF1) levels were evaluated using western blotting. The relationship between FTO and ABCF1 was determined using RNA immunoprecipitation-quantitative polymerase chain reaction (RIPqPCR), MeRIP-qPCR, and RNA stability assays. Echocardiography and Masson\u2019s trichrome and hematoxylineosin staining were used to measure myocardial injury.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"st3\">\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>\n                      FTO expression was reduced in infarcted myocardial tissue and OGD-induced HUVECs (\n                      <jats:italic>P<\/jats:italic>\n                      &lt; 0.01). Functionally, FTO overexpression improved the impaired function of OGD-treated HUVECs and restored myocardial function in MI mice (\n                      <jats:italic>P<\/jats:italic>\n                      &lt; 0.01). Mechanistically, FTO reduced m6A methylation of ABCF1 mRNA and raised ABCF1 levels in OGD-treated HUVECs (\n                      <jats:italic>P<\/jats:italic>\n                      &lt; 0.01).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"st4\">\n                    <jats:title>Conclusion:<\/jats:title>\n                    <jats:p>Taken together, our study revealed that FTO overexpression restored OGD-induced endothelial dysfunction and myocardial pathological injury after MI. FTO increased ABCF1 expression in OGD-treated HUVECs through an m6A-dependent mechanism. These findings offer new insights into mitigating EC dysfunction and myocardial injury after MI.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.25259\/cytojournal_97_2025","type":"journal-article","created":{"date-parts":[[2026,6,5]],"date-time":"2026-06-05T12:25:25Z","timestamp":1780662325000},"page":"35","update-policy":"https:\/\/doi.org\/10.25259\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Fat mass and obesity-associated gene overexpression ameliorates endothelial dysfunction after myocardial infarction by mediating N6-methyladenosine modification of ATP-binding cassette subfamily F member 1"],"prefix":"10.25259","volume":"23","author":[{"given":"Huichao","family":"Pan","sequence":"first","affiliation":[{"name":"Department of Cardiology, The Fourth Affiliated Hospital of Soochow University, Suzhou Dushu Lake Hospital, Medical Center of Soochow University, Suzhou, China,"},{"name":"Department of Cardiology, Tongren Hospital, Shanghai, China,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xunlong","family":"Xu","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Tongren Hospital, Shanghai, China,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yamei","family":"Yu","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Tongren Hospital, Shanghai, China,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhaohui","family":"Qiu","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Tongren Hospital, Shanghai, China,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yafeng","family":"Zhou","sequence":"additional","affiliation":[{"name":"Department of Cardiology, The Fourth Affiliated Hospital of Soochow University, Suzhou Dushu Lake Hospital, Medical Center of Soochow University, Suzhou, 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