{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T19:03:40Z","timestamp":1791486220124,"version":"4.3.4"},"reference-count":60,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"9","license":[{"start":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T00:00:00Z","timestamp":1791504000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation Research"],"published-print":{"date-parts":[[2026,10,9]]},"abstract":"<jats:sec>\n                    <jats:title>BACKGROUND:<\/jats:title>\n                    <jats:p>With obesity as a risk factor for atherosclerotic disease, recent research suggests that adipose tissue in obese animal models and humans can generate endocrine-like molecules that affect arterial health. Previous studies showed that microRNA-30e (miR-30e) levels are elevated in atherosclerosis and solute carrier family 7 member 11 (SLC7A11), a cystine\/glutamate transporter, is involved in atherogenesis. However, whether an endocrine-like link between the adipose-derived miR-30e-5p and SLC7A11 in the vascular endothelium can lead to obesity-caused atherosclerosis is unknown.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS:<\/jats:title>\n                    <jats:p>\n                      miRNA data mining and reverse transcription-polymerase chain reaction validations were used to demonstrate the positive association among serum levels of miR-30e-5p, obesity, and coronary arterial disease in human patients. Transcriptomics (bulk RNA sequencing and single-nucleus RNA sequencing), metabolomics, and in silico analysis were used to establish a miR-30e-5p\u2013SLC7A11 regulation of central carbon metabolism, mitochondrial and endothelial cell (EC) function. Mouse models with EC-specific\n                      <jats:italic toggle=\"yes\">Slc7a11<\/jats:italic>\n                      knockout (EC-\n                      <jats:italic toggle=\"yes\">Slc7a11<\/jats:italic>\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      ) and gain- or loss-of- function of miR-30e-5p were used to elucidate the detrimental role of this endocrine-like axis in obesity-related atherosclerosis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS:<\/jats:title>\n                    <jats:p>\n                      The level of adipocyte-derived miR-30e-5p was significantly upregulated in obese human patients with coronary artery disease and in obese and atherosclerotic mice. Mediated through serum exosomes, the adipocyte-generated miR-30e-5p targeted\n                      <jats:italic toggle=\"yes\">SLC7A11<\/jats:italic>\n                      mRNA in vascular ECs. SLC7A11 deficiency due to miR-30e-5p targeting dysregulated glutamate\/cystine metabolism, increased glycolysis, reduced oxidative phosphorylation, and impaired mitochondrial function. The EC dysfunction could be rectified by SLC7A11 overexpression or miR-30e-5p antagonism. Administration of exogenous miR-30e-5p or white adipose tissue-derived exosomes phenocopied the increased atherosclerosis in EC-\n                      <jats:italic toggle=\"yes\">Slc7a11<\/jats:italic>\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      mice. In contrast, miR-30e-5p antagomir or GW4869 treatment reduced atherosclerosis in\n                      <jats:italic toggle=\"yes\">Apoe<\/jats:italic>\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      and\n                      <jats:italic toggle=\"yes\">ob\/ob<\/jats:italic>\n                      mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS:<\/jats:title>\n                    <jats:p>\n                      Our multiomics approaches demonstrate that the adipose-derived miR-30e-5p downregulated\n                      <jats:italic toggle=\"yes\">SLC7A11<\/jats:italic>\n                      mRNA in ECs via tissue crosstalk. The resulting EC dysfunction led to obesity-related atherosclerosis in mice. These findings underscore a causality between obesity and atherosclerosis in the context of cardiovascular-kidney-metabolic syndrome.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/circresaha.126.328493","type":"journal-article","created":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T09:00:17Z","timestamp":1789117217000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":0,"title":["Obesity Increases Atherosclerosis Susceptibility via an Intertissue miR-30e-SLC7A11 Axis"],"prefix":"10.1161","volume":"139","author":[{"given":"Chen","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Cardiology (C.W., J.S., H.W., X.L., N.G., S.H., J.Z., Y. Lei, X.Z., H. Li, Y. Luo, S.G., X.Y., T.B., Y.X., Z.-Y.Y.), The First Affiliated Hospital of Xi\u2019an Jiaotong University, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jianqing","family":"She","sequence":"additional","affiliation":[{"name":"Department of Cardiology (C.W., J.S., H.W., X.L., N.G., S.H., J.Z., Y. Lei, X.Z., H. Li, Y. Luo, S.G., X.Y., T.B., Y.X., Z.-Y.Y.), The First Affiliated Hospital of Xi\u2019an Jiaotong University, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoli","family":"Qian","sequence":"additional","affiliation":[{"name":"Cardiovascular Research Center, School of Basic Medical Sciences, Xi\u2019an Jiaotong University Health Science Center, China (X.Q., W.H., F.H.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9129-7150","authenticated-orcid":true,"given":"Haoyu","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Cardiology (C.W., J.S., H.W., X.L., N.G., S.H., J.Z., Y. Lei, X.Z., H. Li, Y. 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