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Condition: Heart Failure

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Total 253 results found since Jan 2013.

Resveratrol-enhanced autophagic flux ameliorates myocardial oxidative stress injury in diabetic mice.
Abstract Autophagic dysfunction is observed in diabetes mellitus. Resveratrol has a beneficial effect on diabetic cardiomyopathy. Whether the resveratrol-induced improvement in cardiac function in diabetes is via regulating autophagy remains unclear. We investigated the mechanisms underlying resveratrol-mediated protection against heart failure in diabetic mice, with a focus on the role of sirtuin 1 (SIRT1) in regulating autophagic flux. Diabetic cardiomyopathy in mice was induced by streptozotocin (STZ). Long-term resveratrol treatment improved cardiac function, ameliorated oxidative injury and reduced apoptosis ...
Source: J Cell Mol Med - June 1, 2014 Category: Molecular Biology Authors: Wang B, Yang Q, Sun YY, Xing YF, Wang YB, Lu XT, Bai WW, Liu XQ, Zhao YX Tags: J Cell Mol Med Source Type: research

Resveratrol‐enhanced autophagic flux ameliorates myocardial oxidative stress injury in diabetic mice
Abstract Autophagic dysfunction is observed in diabetes mellitus. Resveratrol has a beneficial effect on diabetic cardiomyopathy. Whether the resveratrol‐induced improvement in cardiac function in diabetes is via regulating autophagy remains unclear. We investigated the mechanisms underlying resveratrol‐mediated protection against heart failure in diabetic mice, with a focus on the role of sirtuin 1 (SIRT1) in regulating autophagic flux. Diabetic cardiomyopathy in mice was induced by streptozotocin (STZ). Long‐term resveratrol treatment improved cardiac function, ameliorated oxidative injury and reduced apoptosis in ...
Source: Journal of Cellular and Molecular Medicine - June 1, 2014 Category: Molecular Biology Authors: Bo Wang, Qing Yang, Yuan‐yuan Sun, Yi‐fan Xing, Ying‐bin Wang, Xiao‐ting Lu, Wen‐wu Bai, Xiao‐qiong Liu, Yu‐xia Zhao Tags: Original Article Source Type: research

High glucose induces smad activation via the transcriptional coregulator p300 and contributes to cardiac fibrosis and hypertrophy
Background: Despite advances in the treatment of heart failure, mortality remains high, particularly in individuals with diabetes. Activated transforming growth factor beta (TGF-beta) contributes to the pathogenesis of the fibrotic interstitium observed in diabetic cardiomyopathy. We hypothesized that high glucose enhances the activity of the transcriptional co-activator p300, leading to the activation of TGF-beta via acetylation of Smad2; and that by inhibiting p300, TGF-beta activity will be reduced and heart failure prevented in a clinically relevant animal model of diabetic cardiomyopathy. Methods: p300 activity was as...
Source: Cardiovascular Diabetology - May 5, 2014 Category: Cardiology Authors: Antoinette Bugyei-TwumAndrew AdvaniSuzanne AdvaniYuan ZhangKerri ThaiDarren KellyKim Connelly Source Type: research

In Vivo Silencing of the Transcription Factor IRF5 Reprograms the Macrophage Phenotype and Improves Infarct Healing
ObjectivesThe aim of this study was to test whether silencing of the transcription factor interferon regulatory factor 5 (IRF5) in cardiac macrophages improves infarct healing and attenuates post–myocardial infarction (MI) remodeling.BackgroundIn healing wounds, the M1 toward M2 macrophage phenotype transition supports resolution of inflammation and tissue repair. Persistence of inflammatory M1 macrophages may derail healing and compromise organ functions. The transcription factor IRF5 up-regulates genes associated with M1 macrophages.MethodsHere we used nanoparticle-delivered small interfering ribonucleic acid (siRNA) ...
Source: Journal of the American College of Cardiology: Cardiovascular Imaging - April 14, 2014 Category: Radiology Source Type: research

Gelsolin (GSN) induces cardiomyocyte hypertrophy and BNP expression via p38 signaling and GATA-4 transcriptional factor activation.
In this study, we used H9c2 and H9c2-GSN stable clones in an attempt to understand the mechanisms of GSN overexpression in cardiomyocytes. These data showed that the overexpression of GSN in H9c2-induced cardiac hypertrophy and increased the pathological hypertrophy markers atrial natriuretic peptide brain natriuretic peptide. Furthermore, we found that E-cadherin expression decreased with the overexpression of GSN in H9c2, but β-catenin expression increased. These data presume that the cytoskeleton is loose. Further, previous studies show that the mitogen-activated protein kinase pathway can induce cardiac hypertrophy. O...
Source: Molecular and Cellular Biochemistry - February 7, 2014 Category: Biochemistry Authors: Hu WS, Ho TJ, Pai P, Chung LC, Kuo CH, Chang SH, Tsai FJ, Tsai CH, Jie YC, Liou YM, Huang CY Tags: Mol Cell Biochem Source Type: research

Apelin inhibits the proliferation and migration of rat PASMCs via the activation of PI3K/Akt/mTOR signal and the inhibition of autophagy under hypoxia
This study provides the evidence that exogenous apelin treatment contributes to inhibit the proliferation and migration of PASMCs by regulating the level of autophagy.
Source: Journal of Cellular and Molecular Medicine - January 22, 2014 Category: Molecular Biology Authors: Hongyu Zhang, Yongsheng Gong, Zhouguang Wang, Liping Jiang, Ran Chen, Xiaofang Fan, Huanmian Zhu, Liping Han, Xiaokun Li, Jian Xiao, Xiaoxia Kong Tags: Original Article Source Type: research

Apelin inhibits the proliferation and migration of rat PASMCs via the activation of PI3K/Akt/mTOR signal and the inhibition of autophagy under hypoxia.
This study provides the evidence that exogenous apelin treatment contributes to inhibit the proliferation and migration of PASMCs by regulating the level of autophagy. PMID: 24447518 [PubMed - as supplied by publisher]
Source: J Cell Mol Med - January 22, 2014 Category: Molecular Biology Authors: Zhang H, Gong Y, Wang Z, Jiang L, Chen R, Fan X, Zhu H, Han L, Li X, Xiao J, Kong X Tags: J Cell Mol Med Source Type: research

GRK5 Regulation of NF-{kappa}B Signaling Signal Transduction
G protein-coupled receptor kinase 5 GRK5 plays a key role in regulating cardiac signaling and its expression is increased in heart failure. GRK5 activity in the nucleus of myocytes has been shown to be detrimental in the setting of pressure-overload hypertrophy. The ubiquitous nuclear transcription factor κB (NF-κB) is involved in the regulation of numerous genes in various tissues, and activation of NF-κB has been shown to be associated with heart disease. Herein, we investigated whether GRK5 can specifically regulate the NF-κB signaling pathway in myocytes. We found that overexpression of GRK5 increased the levels of...
Source: Journal of Biological Chemistry - December 13, 2013 Category: Chemistry Authors: Islam, K. N., Bae, J.-W., Gao, E., Koch, W. J. Tags: Gene Regulation Source Type: research

MicroRNA-150 inhibits expression of adiponectin receptor 2 and is a potential therapeutic target in patients with chronic heart failure
Conclusions: MicroRNA-150 counteracts ADIPOR2 up-regulation in CHF and thus may contribute to adiponectin resistance. Targeting microRNA-150 may be a future strategy to restore cardioprotective adiponectin effects.
Source: The Journal of Heart and Lung Transplantation - October 28, 2013 Category: Transplant Surgery Authors: Simone Kreth, Carola Ledderose, Stefanie Schütz, Andres Beiras, Jens Heyn, Florian Weis, Andres Beiras-Fernandez Tags: Featured Articles Source Type: research

Delivery of Nox2-NADPH oxidase siRNA with polyketal nanoparticles for improving cardiac function following myocardial infarction.
This study highlights the potential of polyketals as siRNA delivery vehicles to the MI heart and represents a viable therapeutic approach for targeting oxidative stress. PMID: 23856052 [PubMed - as supplied by publisher]
Source: Biomaterials - July 12, 2013 Category: Materials Science Authors: Somasuntharam I, Boopathy AV, Khan RS, Martinez MD, Brown ME, Murthy N, Davis ME Tags: Biomaterials Source Type: research

O-GlcNAcylation involvement in high glucose-induced cardiac hypertrophy via ERK1/2 and cyclin D2.
In conclusion, O-GlcNAcylation plays a role in high glucose-induced cardiac hypertrophy via ERK1/2 and cyclin D2. PMID: 23665912 [PubMed - as supplied by publisher]
Source: Amino Acids - May 12, 2013 Category: Biochemistry Authors: Ding F, Yu L, Wang M, Xu S, Xia Q, Fu G Tags: Amino Acids Source Type: research

c-Src-dependent MAPKs/AP-1 activation is involved in TNF-α-induced matrix metalloproteinase-9 expression in rat heart-derived H9c2 cells.
Abstract TNF-α plays a critical mediator in the pathogenesis of chronic heart failure contributing to cardiac remodeling and peripheral vascular disturbances. The implication of TNF-α in inflammatory responses has been shown to be mediated through up-regulation of inflammatory genes, including matrix metalloproteinase-9 (MMP-9). However, the detailed mechanisms of TNF-α-induced MMP-9 expression are largely unclear in the heart cells. Here, we demonstrated that in rat embryonic-heart derived H9c2 cells, TNF-α could induce MMP-9 mRNA expression associated with an increase in the secretion of MMP-9, determined by...
Source: Biochemical Pharmacology - January 24, 2013 Category: Drugs & Pharmacology Authors: Yang CM, Lee IT, Lin CC, Wang CH, Cherng WJ, Hsiao LD Tags: Biochem Pharmacol Source Type: research

Electrical field stimulation induces cardiac fibroblast proliferation through the calcineurin-NFAT pathway.
Abstract Most cardiac diseases are associated with fibrosis. Calcineurin (CaN) is regulated by Ca(2+)/calmodulin (CaM). The CaN-NFAT (nuclear factor of activated T cell) pathway is involved in the process of cardiac diseases, such as cardiac hypertrophy, but its effect on myocardial fibrosis remains unclear. The present study investigates whether the CaN-NFAT pathway is involved in cardiac fibroblast (CF) proliferation induced by electrical field stimulation (EFS), which recently became a popular treatment for heart failure and cardiac tissue engineering. CF proliferation was evaluated by a cell survival assay (MT...
Source: Canadian Journal of Physiology and Pharmacology - December 1, 2012 Category: Drugs & Pharmacology Authors: Chen QQ, Zhang W, Chen XF, Bao YJ, Wang J, Zhu WZ Tags: Can J Physiol Pharmacol Source Type: research