TXNIP公司
拜瑞妥
血管紧张素II
医学
心脏纤维化
心力衰竭
心功能曲线
药理学
心室重构
内科学
内分泌学
氧化应激
受体
硫氧还蛋白
心房颤动
华法林
作者
Yamin Rao,Jing Chen,Yao-Xing Guo,Tao Ji,Ping Xie
标识
DOI:10.1016/j.thromres.2020.05.030
摘要
As an anticoagulant, Rivaroxaban has recently been reported to be protective in cardiac injury. Based on those previous research results, we detected the roles of Rivaroxaban in Angiotensin II (AngII)-induced cardiac remodeling with KKAy mice and unraveled the underlying mechanisms. Rivaroxaban inhibited cardiac fibrosis and hypertrophy in AngII-infused KKAy mice. In addition, it also inhibited mitochondrial dysfunction. Noteworthily, Rivaroxaban altered the expression of many genes associated with mitochondrial function. Rivaroxaban inhibited the expression of thioredoxin binding protein (TXNIP) as well as the activation of apoptosis stimulating kinase 1 (ASK1). In H9c2 cells treated with AngII and high glucose, Rivaroxaban inhibited TXNIP/thioredoxin2 (Trx2) interaction. Moreover, TXNIP knockout abolished AngII-induced cardiac fibrosis and hypertrophy. Thus, Rivaroxaban ameliorates AngII-induced cardiac remodeling via the suppression of TXNIP signaling in KKAy mice, providing novel mechanism underlying the protective roles of Rivaroxaban against cardiac damage.
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