Original articleInhibition by angiotensin II type 1 receptor antagonist of cardiac phenotypic modulation after myocardial infarction
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Autophagy, dysglycemia and myocardial infarction
2017, IJC Metabolic and EndocrineAngiotensin II type 1 receptor antagonists in animal models of vascular, cardiac, metabolic and renal disease
2016, Pharmacology and TherapeuticsCitation Excerpt :Similarly, irbesartan treatment for 7.5 months had little effect on subendocardial fibrosis despite reducing hypertrophy (Richer et al., 1999). Correspondingly, candesartan or cilazapril only inconsistently inhibited the increased expression of collagen I and III after myocardial infarction (Hanatani et al., 1995; Yoshiyama et al., 1999). On the other hand, losartan fully prevented fibrosis induced by myocardial infarction (Smits et al., 1992) and a minor but dose-dependent reduction of fibrosis was observed with azilsartan treatment in a mouse infarction model (Nakamura et al., 2013).
Genetic predisposition to left ventricular dysfunction: A multigenic and multi-analytical approach
2014, GeneCitation Excerpt :While ventricular remodeling is initially a compensatory response, the transition to adverse remodeling frequently culminates in the development of congestive heart failure (CHF) which significantly contributes towards cardiovascular morbidity and mortality rates (Sutton and Sharpe, 2000). The renin–angiotensin–aldosterone system (RAAS), matrix metalloproteinases (MMPs), and inflammatory pathways have been shown to be involved in many cardiovascular diseases, including myocardial fibrosis and hypertrophy, congestive heart failure, myocardial infarction, and cardiomyopathy (Deschamps and Spinale, 2006; Hanatani et al., 1995; Kuusisto et al., 2012; Weber et al., 1993). Among the pathways that contribute to ECM (extracellular matrix) remodeling, the MMPs appear to be of particular interest.
MiRNA-208a and miRNA-208b are triggered in thyroid hormone-induced cardiac hypertrophy - Role of type 1 Angiotensin II receptor (AT1R) on miRNA-208a/α-MHC modulation
2013, Molecular and Cellular EndocrinologyThe effects of NK4 on viral myocarditis mice
2009, Cardiovascular PathologyCitation Excerpt :Thus, tissue fibrosis is regulated by a balance in TGF-β and HGF production. Activation of Ang II is also believed to play an important role in the pathogenesis of fibrosis in cardiovascular disease [28–31]. In an ischemic rat heart, locally generated Ang II is correlated to TGF-β1 expression and synthesis [28], suggesting a concerted action of these two factors.