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Condition: Heart Failure
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Total 161 results found since Jan 2013.

Anti-Inflammatory Peptides From Cardiac Progenitors Ameliorate Dysfunction After Myocardial Infarction Heart Failure
Conclusions Soluble JAM-A secreted from cardiac progenitor cells reduces infiltration of neutrophils after myocardial infarction and ameliorates tissue damage through prevention of excess inflammation. Our finding may lead to a new therapy for cardiovascular disease by using the anti-inflammatory effect of JAM-A.
Source: JAHA:Journal of the American Heart Association - December 2, 2014 Category: Cardiology Authors: Liu, M.-L., Nagai, T., Tokunaga, M., Iwanaga, K., Matsuura, K., Takahashi, T., Kanda, M., Kondo, N., Naito, A. T., Komuro, I., Kobayashi, Y. Tags: Heart Failure Source Type: research

Dyssynchronous Pacing Triggers Endothelial-Mesenchymal Transition Through Heterogeneity of Mechanical Stretch in a Canine Model.
Conclusions:RVP-induced DHF could aggravate fibrosis due to regional heterogeneity of mechanical stress, and it was better in the BiVP group where mechanical stress-induced EndMT might play a pivotal role through the integrin β1 pathway. PMID: 25373595 [PubMed - as supplied by publisher]
Source: Circulation Journal - November 6, 2014 Category: Cardiology Authors: Mai J, Hu Q, Xie Y, Su S, Qiu Q, Yuan W, Yang Y, Song E, Chen Y, Wang J Tags: Circ J Source Type: research

Genistein alleviates pressure overload‐induced cardiac dysfunction and interstitial fibrosis in mice
CONCLUSIONS AND IMPLICATIONSGen improved cardiac function and inhibited cardiac fibrosis in response to pressure overload. The underlying mechanism may involve regulation of the MTA3/TAK1/MKK4/JNK signaling pathway. Gen may serve as a novel agent for prevention and therapy of cardiac disorders associated with fibrosis.
Source: British Journal of Pharmacology - November 3, 2014 Category: Drugs & Pharmacology Authors: Wei Qin, Ning Du, Longyin Zhang, Xianxian Wu, Yingying Hu, Xiaoguang Li, Nannan Shen, Yang Li, Baofeng Yang, Chaoqian Xu, Zhiwei Fang, Yanjie Lu, Yong Zhang, Zhimin Du Tags: Research Paper – Chinese innovation in cardiovascular drug Discovery Themed Issue Source Type: research

Improving heart function by modulating myocardiocyte autophagy: a possible novel mechanism for cardiovascular protection of high-density lipoprotein
Background: High-density lipoprotein (HDL) has been shown to confer cardiovascular protection in clinical and epidemiologic studies. Emerging evidence suggests that many of the cardioprotective functions of HDL may be due to the phospholipid sphingosine-1-phosphate (S1P).Presentation of the hypothesisHDL-S1P binds to S1P receptors in the heart, activating PI3K/Akt signaling and myocyte survival. PI3K/Akt is a classic signaling modulator of autophagy. Excessive autophagy due to cell death and cardiomyocyte loss may contribute to impaired heart function during pressure overload-induced heart failure. Therefore, we hypothesiz...
Source: Lipids in Health and Disease - October 22, 2014 Category: Lipidology Authors: Fan WangPing Ye 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

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

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