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Condition: Heart Failure

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Total 253 results found since Jan 2013.

Evidence for the Role of BAG3 in Mitochondrial Quality Control in Cardiomyocytes
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Source: Journal of Cellular Physiology - July 7, 2016 Category: Cytology Authors: Farzaneh G. Tahrir, Tijana Knezevic, Manish K. Gupta, Jennifer Gordon, Joseph Y. Cheung, Arthur M. Feldman, Kamel Khalili Tags: Original Research Article Source Type: research

Aldosterone and Store-operated Ca2+ Channels Cell Biology
Store-operated Ca2+ entry (SOCE) has emerged as an important mechanism in cardiac pathology. However, the signals that up-regulate SOCE in the heart remain unexplored. Clinical trials have emphasized the beneficial role of mineralocorticoid receptor (MR) signaling blockade in heart failure and associated arrhythmias. Accumulated evidence suggests that the mineralocorticoid hormone aldosterone, through activation of its receptor, MR, might be a key regulator of Ca2+ influx in cardiomyocytes. We thus assessed whether and how SOCE involving transient receptor potential canonical (TRPC) and Orai1 channels are regulated by aldo...
Source: Journal of Biological Chemistry - June 16, 2016 Category: Chemistry Authors: Sabourin, J., Bartoli, F., Antigny, F., Gomez, A. M., Benitah, J.-P. Tags: Cell Biology Source Type: research

The H19 long noncoding RNA is a novel negative regulator of cardiomyocyte hypertrophy
Conclusion These findings reveal a novel function of H19-miR-675 axis targeting CaMKII as a negative regulator of cardiac hypertrophy, suggesting its potential therapeutic role in cardiac diseases.
Source: Cardiovascular Research - June 14, 2016 Category: Cardiology Authors: Liu, L., An, X., Li, Z., Song, Y., Li, L., Zuo, S., Liu, N., Yang, G., Wang, H., Cheng, X., Zhang, Y., Yang, X., Wang, J. Tags: Cardiac biology and remodelling Source Type: research

PT167 RU360 Adsorption in Silica Nanovectors: Potential Use Against Mitochondrial Dysfunction in Heart Failure
Heart failure is the clinical syndrome causing the highest number of adult deaths in industrialized countries, with an annual death rate of 20-40% of the diagnosed cases. There are numerous candidates for heart failure therapy involving regulation of mitochondrial calcium ([Ca2+]m) through the Mitochondrial Calcium Uniporter (MCU), such as the use of Ru360 for inhibition or gene silencing using siRNA. However, their bioavailability is low. Recently, the use of nanovectors as means for drug delivery have been explored given that those could increase the drug bioavailability along with time-programmed drug release.
Source: CVD Prevention and Control - May 31, 2016 Category: Global & Universal Authors: O. Lozano, Y. Oropeza, N. Ornelas, F. Contreras, E. Guerrero-Beltr án, E. Vázquez-Garza, S.E. Cárdenas, G. Torre-Amione, G. García-Rivas Tags: Poster Abstract Source Type: research

Tumor necrosis factor-{alpha} impairs adiponectin signalling, mitochondrial biogenesis, and myogenesis in primary human myotubes cultures
Skeletal muscle metabolic changes are common in patients with chronic heart failure (HF). Previously, we demonstrated a functional skeletal muscle adiponectin resistance in HF patients with reduced left ventricular ejection fraction (HFrEF). We aimed to examine the impact of adiponectin receptor 1 (AdipoR1) deficiency and TNF-α treatment on adiponectin signaling, proliferative capacity, myogenic differentiation, and mitochondrial biogenesis in primary human skeletal muscle cells. Primary cultures of myoblasts and myotubes were initiated from the musculus vastus lateralis of 10 HFrEF patients (left ventricular ejectio...
Source: AJP: Heart and Circulatory Physiology - April 30, 2016 Category: Cardiology Authors: Sente, T., Van Berendoncks, A. M., Fransen, E., Vrints, C. J., Hoymans, V. Y. Tags: ENERGETICS AND METABOLISM Source Type: research

Macrophage migration inhibitory factor promotes cardiac stem cell proliferation and endothelial differentiation through the activation of the PI3K/Akt/mTOR and AMPK pathways.
In conclusion, our results suggest that MIF promotes mCSC survival, proliferation and endothelial differentiation through the activation of the PI3K/Akt/mTOR and AMPK signaling pathways. Thus, MIF may prove to be a potential therapeutic factor in the treatment of heart failure and myocardial infarction by activating CSCs. PMID: 27035848 [PubMed - as supplied by publisher]
Source: International Journal of Molecular Medicine - March 28, 2016 Category: Molecular Biology Authors: Cui J, Zhang F, Wang Y, Liu J, Ming X, Hou J, Lv B, Fang S, Yu B Tags: Int J Mol Med Source Type: research

Endostatin is protective against monocrotaline-induced right heart disease through the inhibition of T-type Ca(2+) channel.
Abstract Endostatin (ES), a C-terminal fragment of collagen XVIIIα1, has a potent anti-angiogenic effect. ES prevents tumor proliferation through inhibiting T-type Ca(2+) channel. T-type Ca(2+) channel is re-expressed during heart diseases including monocrotaline (MCT)-induced right heart failure. The present study aimed to clarify the effects of ES on T-type Ca(2+) channel and pathogenesis of MCT-induced right ventricular disease. MCT or saline was injected intraperitoneally to rats. After cardiomyocytes were isolated from right ventricles (RVs), T-type Ca(2+) channel current (I CaT) was measured by a patch-clam...
Source: Pflugers Archiv : European Journal of Physiology - March 28, 2016 Category: Physiology Authors: Imoto K, Kumatani S, Okada M, Yamawaki H Tags: Pflugers Arch Source Type: research

ERK1/2 MAPK signaling in hypothalamic paraventricular nucleus contributes to sympathetic excitation in rats with heart failure after myocardial infarction
Brain MAPK signaling pathways are activated in heart failure (HF) induced by myocardial infarction and contribute to augmented sympathetic nerve activity. We tested whether decreasing ERK1/2 (also known as p44/42 MAPK) signaling in the hypothalamic paraventricular nucleus (PVN), a forebrain source of presympathetic neurons, would reduce the upregulation of sympathoexcitatory mediators in the PVN and augmented sympathetic nerve activity in rats with HF. Sprague-Dawley rats underwent left anterior descending coronary artery ligation to induce HF, with left ventricular dysfunction confirmed by echocardiography. One week after...
Source: AJP: Heart and Circulatory Physiology - March 15, 2016 Category: Cardiology Authors: Yu, Y., Wei, S.-G., Zhang, Z.-H., Weiss, R. M., Felder, R. B. Tags: CARDIOVASCULAR NEUROHORMONAL REGULATION Source Type: research

The TIR/BB-loop mimetic AS-1 attenuates mechanical stress-induced cardiac fibroblast activation and paracrine secretion via modulation of large tumor suppressor kinase 1
Publication date: Available online 7 March 2016 Source:Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease Author(s): Min Fan, Juan Song, Yijie He, Xin Shen, Jiantao Li, Linli Que, Guoqing Zhu, Quan Zhu, Xin Cai, Tuanzhu Ha, Qi Chen, Yong Xu, Chuanfu Li, Yuehua Li The TIR/BB-loop mimetic AS-1 has been reported to prevent cardiac hypertrophy by inhibiting interleukin-1 receptor (IL-1R)-mediated myeloid differentiation primary response gene 88 (MyD88)-dependent signaling. To date, it remains unknown whether and if so how AS-1 contributes to mechanical stress (MS)-induced cardiac fibroblast activa...
Source: Biochimica et Biophysica Acta (BBA) Molecular Basis of Disease - March 8, 2016 Category: Molecular Biology Source Type: research

The TIR/BB-loop mimetic AS-1 attenuates mechanical stress-induced cardiac fibroblast activation and paracrine secretion via modulation of large tumor suppressor kinase 1.
Abstract The TIR/BB-loop mimetic AS-1 has been reported to prevent cardiac hypertrophy by inhibiting interleukin-1 receptor (IL-1R)-mediated myeloid differentiation primary response gene 88 (MyD88)-dependent signaling. To date, it remains unknown whether and if so how AS-1 contributes to mechanical stress (MS)-induced cardiac fibroblast activation, a key process in pressure overload-induced cardiac remodeling and heart failure. Here, we show that phosphorylation and expression of large tumor suppressor kinase 1 (LATS1), a key molecule in the Hippo-Yes associated protein (YAP) signaling pathway, were down-regulated...
Source: Biochimica et Biophysica Acta - March 7, 2016 Category: Biochemistry Authors: Fan M, Song J, He Y, Shen X, Li J, Que L, Zhu G, Zhu Q, Cai X, Ha T, Chen Q, Xu Y, Li C, Li Y Tags: Biochim Biophys Acta Source Type: research

Tumor necrosis factor-α impairs adiponectin signalling, mitochondrial biogenesis and myogenesis in primary human myotubes cultures.
CONCLUSION: Major features of adiponectin resistance are retained in primary cultures from the skeletal muscle of HFrEF patients. In addition, our results suggest that an increased inflammatory constitution contributes to adiponectin resistance and confers alterations in skeletal muscle differentiation, growth and function. PMID: 26921438 [PubMed - as supplied by publisher]
Source: American Journal of Physiology. Heart and Circulatory Physiology - February 26, 2016 Category: Physiology Authors: Sente T, Van Berendoncks AM, Fransen E, Vrints CJ, Hoymans VY Tags: Am J Physiol Heart Circ Physiol Source Type: research

ERK1/2 MAPK Signaling in Hypothalamic Paraventricular Nucleus Contributes to Sympathetic Excitation in Rats with Heart Failure after Myocardial Infarction.
Abstract Brain mitogen-activated protein kinase (MAPK) signaling pathways are activated in heart failure (HF) induced by myocardial infarction and contribute to augmented sympathetic nerve activity. We tested whether silencing brain extracellular signal-regulated kinases 1 and 2 (ERK1/2, also known as p44/42 MAPK) in the hypothalamic paraventricular nucleus (PVN), a forebrain source of presympathetic neurons, would reduce the upregulation of sympatho-excitatory mediators in the PVN and the augmented sympathetic nerve activity in rats with HF. Sprague-Dawley rats underwent left anterior descending coronary artery l...
Source: American Journal of Physiology. Heart and Circulatory Physiology - January 22, 2016 Category: Physiology Authors: Yu Y, Wei SG, Zhang ZH, Weiss RM, Felder RB Tags: Am J Physiol Heart Circ Physiol Source Type: research

MicroRNA-503 promotes angiotensin II-induced cardiac fibrosis by targeting Apelin-13.
This study aimed to explore the role of miR-503 and its mechanisms in regulating cardiac fibrosis. miR-503 was found up-regulated in the mouse LV tissues subjected to transverse aortic constriction (TAC) and in neonatal cardiac fibroblasts (CFs) cultured with Angiotension II. The role of miR-503 in regulating CF cell proliferation and/or collagen production in mice neonatal CFs were determined using an MTT assay and RT-PCR respectively. Forced expression of miR-503 increased the cellular proliferation and collagen production in mice neonatal CFs. The effects were abrogated by cotransfection with AMO-503 (a specific inhibit...
Source: J Cell Mol Med - January 12, 2016 Category: Molecular Biology Authors: Zhou Y, Deng L, Zhao D, Chen L, Yao Z, Guo X, Liu X, Lv L, Leng B, Xu W, Qiao G, Shan H Tags: J Cell Mol Med Source Type: research

Regulation of mitochondrial oxidative stress by {beta}-arrestins in cultured human cardiac fibroblasts RESEARCH ARTICLE
ABSTRACT Oxidative stress in cardiac fibroblasts (CFs) promotes transformation to myofibroblasts and collagen synthesis leading to myocardial fibrosis, a precursor to heart failure (HF). NADPH oxidase 4 (Nox4) is a major source of cardiac reactive oxygen species (ROS); however, mechanisms of Nox4 regulation are unclear. β-arrestins are scaffold proteins that signal in G-protein-dependent and -independent pathways; for example, in ERK activation. We hypothesize that β-arrestins regulate oxidative stress in a Nox4-dependent manner and increase fibrosis in HF. CFs were isolated from normal and failing adult human le...
Source: DMM Disease Models and Mechanisms - December 4, 2015 Category: Biomedical Science Authors: Philip, J. L., Razzaque, M. A., Han, M., Li, J., Theccanat, T., Xu, X., Akhter, S. A. Tags: RESEARCH ARTICLE Source Type: research