منابع مشابه
S100A1 in human heart failure: lack of recovery following left ventricular assist device support.
BACKGROUND We hypothesized that S100A1 is regulated during human hypertrophy and heart failure and that it may be implicated in remodeling after left ventricular assist device. S100A1 is decreased in animal and human heart failure, and restoration produces functional recovery in animal models and in failing human myocytes. With the potential for gene therapy, it is important to carefully explor...
متن کاملS100A1: Another Step Toward Therapeutic Development for Heart Failure.
It has been nearly 130 years since Sydney Ringer’s astute observations on the indispensability of extracellular Ca to eart muscle contraction (1). At the cellular level, we now now that fluctuations of cytosolic Ca are coordinated by everal myocyte proteins in order to functionally couple the ardiac action potential to sarcomeric shortening and mitohondrial energy production. This elegant myoca...
متن کاملStable myocardial-specific AAV6-S100A1 gene therapy results in chronic functional heart failure rescue.
BACKGROUND The incidence of heart failure is ever-growing, and it is urgent to develop improved treatments. An attractive approach is gene therapy; however, the clinical barrier has yet to be broken because of several issues, including the lack of an ideal vector supporting safe and long-term myocardial transgene expression. METHODS AND RESULTS Here, we show that the use of a recombinant aden...
متن کاملCardiac AAV9-S100A1 gene therapy rescues post-ischemic heart failure in a preclinical large animal model.
As a prerequisite for clinical application, we determined the long-term therapeutic effectiveness and safety of adeno-associated virus (AAV)-S100A1 gene therapy in a preclinical large animal model of heart failure. S100A1, a positive inotropic regulator of myocardial contractility, becomes depleted in failing cardiomyocytes in humans and animals, and myocardial-targeted S100A1 gene transfer res...
متن کاملS100A1 transgenic treatment of acute heart failure causes proteomic changes in rats
S100 Ca2+-binding protein A1 (S100A1) is an important regulator of myocardial contractility. The aim of the present study was to identify the underlying mechanisms of S100A1 activity via profiling the protein expression in rats administered with an S100A1 adenovirus (Ad‑S100A1‑EGFP) following acute myocardial infarction (AMI). LTQ OrbiTrap mass spectrometry was used to profile the protein expre...
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ژورنال
عنوان ژورنال: Circulation: Heart Failure
سال: 2014
ISSN: 1941-3289,1941-3297
DOI: 10.1161/circheartfailure.113.000849