Key result
Salusin-β knockdown improved endothelial function, cardiac function, and cardiovascular remodeling in CHF rats by inhibiting NAD(P)H oxidase-ROS generation and activating eNOS-NO production.
Why the study?
The regulatory effects of salusin-β in myocardial infarction-induced chronic heart failure were unknown.
Does salusin-β knockdown improve cardiovascular function in myocardial infarction-induced chronic heart failure rats?
Does salusin-β knockdown improve cardiovascular function in myocardial infarction-induced chronic heart failure rats?
Knockdown of salusin-β improves endothelial and cardiac function in a rat model of chronic heart failure, suggesting a potential novel therapeutic target.
Does not support clinical use in heart failure; leaves open salusin-β as a translational target.
Salusin‐β is a biologically active peptide with 20 amino acids that exerts several cardiovascular activity‐regulating effects, such as regulating vascular endothelial function and the proliferation of vascular smooth muscle cells. However, the regulatory effects of salusin‐β in myocardial infarction‐induced chronic heart failure (CHF) are still unknown. The current study is aimed at investigating the effects of silencing salusin‐β 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‐operated (Sham) rats were subjected to tail vein injection of adenoviral vectors encoding salusin‐β shRNA or a control‐shRNA. 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‐β, leptin and visfatin levels and the salusin‐β protein expression levels of CA, PA, and MA were increased, while the acetylcholine‐ (ACh‐) induced endothelium‐dependent vascular relaxation of CA, PA, and MA was attenuated significantly in CHF rats and was improved significantly by salusin‐β gene knockdown. Salusin‐β 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‐2 and NOX‐4 expression, and reactive oxygen species (ROS) levels in arteries in CHF rats. The effects of salusin‐β knockdown in CHF rats were attenuated significantly by pretreatment with the NOS inhibitor L‐NAME. These results indicate that silencing salusin‐β contributes to the improvement of endothelial function, cardiac function, and cardiovascular remodeling in CHF by inhibiting NAD(P)H oxidase‐ROS generation and activating eNOS‐NO production.
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Xu et al. (2021) studied Myocardial infarction-induced chronic heart failure. Salusin-β gene knockdown (adenoviral vectors encoding salusin-β shRNA) vs. Control-shRNA and sham operation was evaluated on Endothelial function, cardiac function, vascular and myocardial remodeling. Salusin-β knockdown improved endothelial function, cardiac function, and cardiovascular remodeling in CHF rats by inhibiting NAD(P)H oxidase-ROS generation and activating eNOS-NO production.
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