CXCR4 gene transfer prevents pressure overload induced heart failure
نویسندگان
چکیده
منابع مشابه
T cell costimulation blockade blunts pressure overload-induced heart failure
Heart failure (HF) is a leading cause of mortality. Inflammation is implicated in HF, yet clinical trials targeting pro-inflammatory cytokines in HF were unsuccessful, possibly due to redundant functions of individual cytokines. Searching for better cardiac inflammation targets, here we link T cells with HF development in a mouse model of pathological cardiac hypertrophy and in human HF patient...
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BACKGROUND Estrogen pretreatment has been shown to attenuate the development of heart hypertrophy, but it is not known whether estrogen could also rescue heart failure (HF). Furthermore, the heart has all the machinery to locally biosynthesize estrogen via aromatase, but the role of local cardiac estrogen synthesis in HF has not yet been studied. Here we hypothesized that cardiac estrogen is re...
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Transverse aortic constriction (TAC)-induced pressure overload (PO) causes adverse cardiac remodeling and dysfunction that progresses to heart failure (HF). The purpose of this study was to determine whether the potent antioxidant, resveratrol, significantly attenuates PO-induced HF in wild-type mice. Male C57BL6 mice were subjected to either sham or TAC surgery. One group of TAC mice was given...
متن کاملEpigenetic Switch at Atp2a2 and Myh7 Gene Promoters in Pressure Overload-Induced Heart Failure
Re-induction of fetal genes and/or re-expression of postnatal genes represent hallmarks of pathological cardiac remodeling, and are considered important in the progression of the normal heart towards heart failure (HF). Whether epigenetic modifications are involved in these processes is currently under investigation. Here we hypothesized that histone chromatin modifications may underlie changes...
متن کاملEndothelial p53 Deletion Improves Angiogenesis and Prevents Cardiac Fibrosis and Heart Failure Induced by Pressure Overload in Mice
BACKGROUND Cardiac dysfunction developing in response to chronic pressure overload is associated with apoptotic cell death and myocardial vessel rarefaction. We examined whether deletion of tumor suppressor p53 in endothelial cells may prevent the transition from cardiac hypertrophy to heart failure. METHODS AND RESULTS Mice with endothelial-specific deletion of p53 (End.p53-KO) were generate...
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ژورنال
عنوان ژورنال: Journal of Molecular and Cellular Cardiology
سال: 2012
ISSN: 0022-2828
DOI: 10.1016/j.yjmcc.2012.05.016