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Condition: Heart Failure

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Total 253 results found since Jan 2013.

Small interfering RNA therapy against carbohydrate sulfotransferase 15 inhibits cardiac remodeling in rats with dilated cardiomyopathy.
Abstract Carbohydrate sulfotransferase 15 (CHST15) is a sulfotransferase responsible for biosynthesis of chondroitin sulfate E (CS-E), which plays important roles in numerous biological events such as biosynthesis of proinflammatory cytokines. However, the effects of CHST15 siRNA in rats with chronic heart failure (CHF) after experimental autoimmune myocarditis (EAM) have not yet been investigated. CHF was elicited in Lewis rats by immunization with cardiac myosin, and after immunization, the rats were divided into two groups and treated with either CHST15 siRNA (2μg/week) or vehicle. Age matched normal rats with...
Source: Cellular Signalling - March 14, 2015 Category: Cytology Authors: Watanabe K, Arumugam S, Sreedhar R, Thandavarayan RA, Nakamura T, Nakamura M, Harima M, Yoneyama H, Suzuki K Tags: Cell Signal Source Type: research

Qiliqiangxin inhibits angiotensin II-induced transdifferentiation of rat cardiac fibroblasts through suppressing interleukin-6.
This study aimed to investigate the effects of QL on angiotensin II (AngII)-induced CFs transdifferentiation. Study was performed on in vitro cultured CFs from Sprague-Dawley rats. CFs differentiation was induced by AngII, which was attenuated by QL through reducing transforming growth factor-β1 (TGF-β1 ) and α-smooth muscle actin (α-SMA). Our data showed that AngII-induced IL-6 mRNA as well as typeI and typeIII collagens were reduced by QL. IL-6 deficiency could suppress TGF-β1 and α-SMA, and both IL-6 siRNA and QL-mediated such effect was reversed by foresed expression of recombined IL-6. Increase in actin stress f...
Source: J Cell Mol Med - March 6, 2015 Category: Molecular Biology Authors: Zhou J, Jiang K, Ding X, Fu M, Wang S, Zhu L, He T, Wang J, Sun A, Hu K, Chen L, Zou Y, Ge J Tags: J Cell Mol Med Source Type: research

Qiliqiangxin inhibits angiotensin II‐induced transdifferentiation of rat cardiac fibroblasts through suppressing interleukin‐6
This study aimed to investigate the effects of QL on angiotensin II (AngII)‐induced CFs transdifferentiation. Study was performed on in vitro cultured CFs from Sprague–Dawley rats. CFs differentiation was induced by AngII, which was attenuated by QL through reducing transforming growth factor‐β1 (TGF‐β1) and α‐smooth muscle actin (α‐SMA). Our data showed that AngII‐induced IL‐6 mRNA as well as typeI and typeIII collagens were reduced by QL. IL‐6 deficiency could suppress TGF‐β1 and α‐SMA, and both IL‐6 siRNA and QL‐mediated such effect was reversed by foresed expression of recombined IL‐6....
Source: Journal of Cellular and Molecular Medicine - March 6, 2015 Category: Molecular Biology Authors: Jingmin Zhou, Kun Jiang, Xuefeng Ding, Mingqiang Fu, Shijun Wang, Lingti Zhu, Tao He, Jingfeng Wang, Aijun Sun, Kai Hu, Li Chen, Yunzeng Zou, Junbo Ge Tags: Original Article Source Type: research

Silencing collapsin response mediator protein-2 reprograms macrophage phenotype and improves infarct healing in experimental myocardial infarction model
Conclusion: CRMP2 is highly expressed in M1 macrophages and silencing CRMP2 reprograms macrophage phenotype and improves infarct healing in atherosclerotic mice.
Source: Journal of Inflammation - February 10, 2015 Category: Allergy & Immunology Authors: Long-Shu ZhouGuo-Long ZhaoQiang LiuShu-Cai JiangYun WangDong-Mei Zhang Source Type: research

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

Protein phosphatase 2C-alpha knockdown reduces angiotensin II-mediated skeletal muscle wasting via restoration of mitochondrial recycling and function
Conclusions: AngII inhibited AMPK activity and reduced PGC-1α and TFAM expression (thereby inhibiting mitochondrial biogenesis) and impaired ULK1 activation and autophagy (thereby also inhibiting clearance of damaged mitochondria), resulting in mitochondrial dysfunction, decreased ATP, and wasting. Knockdown of PP2Cα normalized AMPK activity, PGC-1α, NRF1, and TFAM levels and blocked AngII inhibition of ULK1, leading to improved mitochondrial biogenesis/recycling/function, energy production, and inhibition of AngII-induced wasting. These results demonstrate novel effects of AngII on cellular metabolism that are likely c...
Source: Skeletal Muscle - October 30, 2014 Category: Research Authors: Alexander TabonyTadashi YoshidaSergiy SukhanovPatrice Delafontaine 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

Contribution of neuronal isoform Nav1.1 to late sodium current in ventricular myocytes from failing hearts.
In conclusion, we have discovered Nav1.1-originated INaL component in dog heart ventricular cells. This component is physiologically relevant to control AP shape and duration, as well as to cell Ca(2+) dynamics. This article is protected by copyright. All rights reserved. PMID: 25326451 [PubMed - as supplied by publisher]
Source: The Journal of Physiology - October 17, 2014 Category: Physiology Authors: Mishra S, Reznikov V, Maltsev VA, Undrovinas NA, Sabbah HN, Undrovinas A Tags: J Physiol Source Type: research

AT2 Receptor Potentiates Skeletal Muscle Regeneration Cell Biology
Patients with advanced congestive heart failure (CHF) or chronic kidney disease (CKD) often have increased angiotensin II (Ang II) levels and cachexia. Ang II infusion in rodents causes sustained skeletal muscle wasting and decreases muscle regenerative potential through Ang II type 1 receptor (AT1R)-mediated signaling, likely contributing to the development of cachexia in CHF and CKD. However, the potential role of Ang II type 2 receptor (AT2R) signaling in skeletal muscle physiology is unknown. We found that AT2R expression was increased robustly in regenerating skeletal muscle after cardiotoxin (CTX)-induced muscle inju...
Source: Journal of Biological Chemistry - September 18, 2014 Category: Chemistry Authors: Yoshida, T., Huq, T. S., Delafontaine, P. Tags: Molecular Bases of Disease Source Type: research

Sumo E2 Ligase UBC9 is Required for Efficient Protein Quality Control in Cardiomyocytes.
Conclusions: UBC9 plays a significant role in cardiomyocyte PQC and its activity can be exploited to reduce toxic levels of misfolded or aggregated proteins in cardiomyopathy. PMID: 25097219 [PubMed - as supplied by publisher]
Source: Circulation Research - August 5, 2014 Category: Cardiology Authors: Gupta MK, Gulick J, Liu R, Wang X, Molkentin JD, Robbins J Tags: Circ Res Source Type: research

Insulin, NF-{kappa}B, and Myocardin Signaling in Cardiac Myoblasts Signal Transduction
Hyperinsulinemia contributes to cardiac hypertrophy and heart failure in patients with the metabolic syndrome and type 2 diabetes. Here, high circulating levels of tumor necrosis factor (TNF)-α may synergize with insulin in signaling inflammation and cardiac hypertrophy. We tested whether high insulin affects activation of TNF-α-induced NF-κB and myocardin/serum response factor (SRF) to convey hypertrophy signaling in cardiac myoblasts. In canine cardiac myoblasts, treatment with high insulin (10−8 to 10−7 m) for 0–24 h increased insulin receptor substrate (IRS)-1 phosphorylation at Ser-307, decreased protein leve...
Source: Journal of Biological Chemistry - July 10, 2014 Category: Chemistry Authors: Madonna, R., Geng, Y.-J., Bolli, R., Rokosh, G., Ferdinandy, P., Patterson, C., De Caterina, R. Tags: Gene Regulation Source Type: research

Cardioprotective Effect of the Selective Sigma-1 Receptor Agonist, SA4503.
Abstract   We previously reported that the sigma-1 receptor is down-regulated in cardiomyocytes following heart failure in transverse aortic constriction (TAC) mice. In this review, we summarized the anti-hypertrophic action of selective sigma-1 receptor agonist, SA4503 in the hypertrophied cultured cardiomyocytes and discussed its possible mechanism of cardioprotection. Treatment with SA4503 (0.1-1 μM) dose-dependently inhibited hypertrophy in cultured cardiomyocytes induced by angiotensin II (Ang II). We also found that α1 receptor stimulation by phenylephrine (PE) promotes ATP production through IP3 recepto...
Source: Yakugaku Zasshi : Journal of the Pharmaceutical Society of Japan - June 8, 2014 Category: Drugs & Pharmacology Authors: Hirano K, Tagashira H, Fukunaga K Tags: Yakugaku Zasshi Source Type: research

Bone Morphogenetic Protein‐10 induces cardiomyocyte proliferation and improves cardiac function after myocardial infarction
Heart disease is among the leading causes of death worldwide, and the limited proliferation of mammalian cardiomyocytes prevents heart regeneration in response to injury. Bone morphogenetic protein‐10 (BMP10) exerts multiple roles in various developmental events; however, the effect of BMP10 and the underlying mechanism involved in cardiac repair remains unclear. After stimulation with the recombinant BMP10, an obvious dose‐dependent cardiomyocyte proliferation and reentry of differentiated mammalian cardiomyocytes into the cell cycle was observed. Furthermore, BMP10 stimulation strikingly enhanced Tbx20 expression. Fu...
Source: Journal of Cellular Biochemistry - June 6, 2014 Category: Biochemistry Authors: Lijun Sun, Jing Yu, Shun Qi, Yuewen Hao, Ying Liu, Zhenwu Li Tags: Article Source Type: research