{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T06:46:45Z","timestamp":1791960405418,"version":"4.3.4"},"reference-count":41,"publisher":"Informa UK Limited","issue":"1","license":[{"start":{"date-parts":[[2021,11,1]],"date-time":"2021-11-01T00:00:00Z","timestamp":1635724800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2021,12,22]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n               <jats:p>Nesfatin-1\u00a0is a neuropeptide produced in the hypothalamus. It is known that Nesfatin-1 is involved in food uptake, fat storage, and other metabolic regulation. We hypothesized that Nesfatin-1 may play a role in cardiovascular tissue. Free fatty acids (FFAs) are known to be the risk factor for cardiovascular diseases. FFA-mediated endothelial dysfunction is the critical mechanism of many cardiovascular disorders. The present study explores the protective effects of Nesfatin-1 on FFA-induced endothelial inflammation and the underlying mechanism. We found that significantly increased lactate dehydrogenase release and production of inflammatory factors were observed in FFA-treated human aortic\u00a0endothelial\u00a0cells (HAECs), accompanied by the enhanced attachment of U937 monocytes to HAECs and upregulated cell adhesion molecule vascular cell adhesion molecule-1, which were dramatically reversed by the treatment with Nesfatin-1. In addition, the promoted level of nuclear regulator NF-\u03baB p65 and transcriptional function of NF-\u03baB in FFA-treated HAECs were greatly suppressed by HAECs. Growth Factor Independent 1 Transcriptional Repressor 1 (Gfi1), an important negative regulator of NF-\u03baB activity, was significantly downregulated in HAECs by FFAs and was upregulated by Nesfatin-1. Lastly, the inhibitory effects of Nesfatin-1 against FFA-induced NF-\u03baB activation and adhesion of U937 monocytes to HAECs were abolished by the knockdown of Gfi1. In conclusion, our data reveal that Nesfatin-1 inhibited FFA-induced endothelial inflammation mediated by the Gfi1\/NF-\u03baB signaling pathway.<\/jats:p>","DOI":"10.1093\/bbb\/zbab186","type":"journal-article","created":{"date-parts":[[2021,11,1]],"date-time":"2021-11-01T14:54:33Z","timestamp":1635778473000},"page":"47-55","source":"Crossref","is-referenced-by-count":13,"title":["Nesfatin-1 inhibits free fatty acid (FFA)-induced endothelial inflammation via Gfi1\/NF-\u03baB signaling"],"prefix":"10.1080","volume":"86","author":[{"given":"Qingtao","family":"Meng","sequence":"first","affiliation":[{"name":"Department of Cardiovascular Surgery, Affiliated Zhongshan Hospital of Dalian University, Dalian, Liaoning, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qin","family":"Lu","sequence":"additional","affiliation":[{"name":"Department of Cardiology, the Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, 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