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However, the regulatory effects of salusin\u2010<jats:italic>\u03b2<\/jats:italic> in myocardial infarction\u2010induced chronic heart failure (CHF) are still unknown. The current study is aimed at investigating the effects of silencing salusin\u2010<jats:italic>\u03b2<\/jats:italic> on endothelial function, cardiac function, vascular and myocardial remodeling, and its underlying signaling pathways in CHF rats induced by coronary artery ligation. CHF and sham\u2010operated (Sham) rats were subjected to tail vein injection of adenoviral vectors encoding salusin\u2010<jats:italic>\u03b2<\/jats:italic> shRNA or a control\u2010shRNA. The coronary artery (CA), pulmonary artery (PA), and mesenteric artery (MA) were isolated from rats, and isometric tension measurements of arteries were performed. Compared with Sham rats, the plasma salusin\u2010<jats:italic>\u03b2<\/jats:italic>, leptin and visfatin levels and the salusin\u2010<jats:italic>\u03b2<\/jats:italic> protein expression levels of CA, PA, and MA were increased, while the acetylcholine\u2010 (ACh\u2010) induced endothelium\u2010dependent vascular relaxation of CA, PA, and MA was attenuated significantly in CHF rats and was improved significantly by salusin\u2010<jats:italic>\u03b2<\/jats:italic> gene knockdown. Salusin\u2010<jats:italic>\u03b2<\/jats:italic> knockdown also improved cardiac function and vascular and myocardial remodeling, increased endothelial nitric oxide synthase (eNOS) activity and nitric oxide (NO) levels, and decreased NAD(P)H oxidase activity, NOX\u20102 and NOX\u20104 expression, and reactive oxygen species (ROS) levels in arteries in CHF rats. The effects of salusin\u2010<jats:italic>\u03b2<\/jats:italic> knockdown in CHF rats were attenuated significantly by pretreatment with the NOS inhibitor L\u2010NAME. These results indicate that silencing salusin\u2010<jats:italic>\u03b2<\/jats:italic> contributes to the improvement of endothelial function, cardiac function, and cardiovascular remodeling in CHF by inhibiting NAD(P)H oxidase\u2010ROS generation and activating eNOS\u2010NO production.<\/jats:p>","DOI":"10.1155\/2021\/8896226","type":"journal-article","created":{"date-parts":[[2021,8,11]],"date-time":"2021-08-11T17:05:06Z","timestamp":1628701506000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Knockdown of Salusin\u2010<i>\u03b2<\/i> Improves Cardiovascular Function in Myocardial Infarction\u2010Induced Chronic Heart Failure 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