Downregulation of @entity766 is Involved in Direct Actions of XXXX on the Heart: Implications for Cardiac @entity82 and Hypertrophy.

@entity712 @entity296 @entity82 @entity2986 @entity19 @entity1283 @entity13436 @entity299 @entity583 @entity766 @entity21243
PURPOSE: @entity296 contributes to @entity299 and loss of cardiac function in @entity583 and @entity712 . This study used in vitro and in vivo models to examine the effects of @entity21243 (UA) on @entity296 and to explore its potential mechanism. METHODS: Transverse aortic constriction (TAC) surgery was performed in @entity19 to induce @entity1283 and @entity82 . UA was orally administered one week prior to TAC. Two weeks after TAC, myocardial pathology was detected using Masson's trichrome staining and transmission electron microscopy, and heart-to-body weight ratio was measured. For in vitro studies, cultured cardiac fibroblasts were treated with serum in the presence or absence of UA. The relative levels of @entity766 and @entity2986 / @entity13436 , collagen content and cell viability were measured. RESULTS: UA attenuated pathological @entity1283 and @entity296 in vivo induced by TAC. Down-regulation of @entity766 and @entity2986 / @entity13436 were observed in myocardial  fibroblasts treated with UA in a dose-dependent manner compared with the control group both in vitro and in vivo. CONCLUSIONS: Our study demonstrates that UA can inhibit @entity296 both in vitro and in vivo, and the effect of UA on @entity296 may be due to the inhibition of @entity766 / @entity13436 signaling pathways. This article is protected by copyright. All rights reserved.
