本文采用的英格恩产品: RNA-Entranster-invivo

Rivaroxaban ameliorates angiotensin II-induced cardiac remodeling by attenuating TXNIP/Trx2 interaction in KKAy mice

Yamin Rao  ¹ , Jing Chen  ¹ , Yaoxing Guo  ¹ , Tianhai Ji  ¹ , Ping Xie  ² Affiliations

• PMID: 32521334
• DOI: 10.1016/j.thromres.2020.05.030

Abstract

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.

Keywords: Angiotension II; Cardiac remodeling; Mitochondria; Rivaroxaban; TXNIP.