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Condition: Heart Failure

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Total 253 results found since Jan 2013.

HDAC11 deletion reduces fructose-induced cardiac dyslipidemia, apoptosis and inflammation by attenuating oxidative stress injury.
Abstract Diabetes mellitus (DM) is a risk factor for abnormal heart development, but the molecular mechanism remains obscure. Histone deacetylase 11 (HDAC11), the most recently identified histone deacetylase, is the sole member of class IV HDACs. However, its role in diabetic cardiac injury is still poorly understood. In the present study, we attempted to explore the effects of HDAC11 on fructose (Fru)-induced cardiac injury using the wild type (HDAC11+/+) and knockout (HDAC11-/-) mice. The results indicated that HDAC11 was significantly expressed in human and mouse diabetic heart failure (DHF) hearts. HDAC11-/- r...
Source: Biochemical and Biophysical Research communications - April 12, 2018 Category: Biochemistry Authors: Fan XD, Wan LL, Duan M, Lu S Tags: Biochem Biophys Res Commun Source Type: research

Abnormal Downregulation of Caveolin-3 Mediates the Pro-Fibrotic Action of MicroRNA-22 in a Model of Myocardial Infarction
Conclusions: Our findings demonstrate that miR-22 accelerates cardiac fibrosis through the miR-22-Cav3-PKC ε pathway, which, therefore, may represent a new therapeutic target for treatment of excessive fibrosis-associated cardiac diseases.Cell Physiol Biochem 2018;45:1641 –1653
Source: Cellular Physiology and Biochemistry - February 27, 2018 Category: Cytology Source Type: research

Bone Morphogenetic Protein 9 Reduces Cardiac Fibrosis and Improves Cardiac Function in Heart Failure.
Conclusions -Our results identify a novel functional role for BMP9 as an endogenous inhibitor of cardiac fibrosis due to LV pressure overload and further show that treatment with either recombinant BMP9 or disruption of endoglin activity promotes BMP9 activity and limits cardiac fibrosis in heart failure, thereby providing potentially novel therapeutic approaches for patients with heart failure. PMID: 29487140 [PubMed - as supplied by publisher]
Source: Circulation - February 27, 2018 Category: Cardiology Authors: Morine KJ, Qiao X, York S, Natov PS, Paruchuri V, Zhang Y, Aronovitz MJ, Karas RH, Kapur NK Tags: Circulation Source Type: research

miR-195 Regulates Metabolism in Failing Myocardium via Alterations in SIRT3 Expression and Mitochondrial Protein Acetylation.
Conclusions -Altogether, these data suggest that increased levels of miR-195 in failing myocardium regulate a novel pathway that involves direct SIRT3 suppression and enzymatic inhibition via increased acetylation of PDH and ATP synthase that are essential for cardiac energy metabolism. PMID: 29330215 [PubMed - as supplied by publisher]
Source: Circulation - January 12, 2018 Category: Cardiology Authors: Zhang X, Ji R, Liao X, Castillero E, Kennel PJ, Brunjes DL, Franz M, Möbius-Winkler S, Drosatos K, George I, Chen EI, Colombo PC, Schulze PC Tags: Circulation Source Type: research

Pathogenic Role of the Damage-Associated Molecular Patterns S100A8 and S100A9 in Coxsackievirus B3-Induced Myocarditis Original Articles
Conclusions: S100A8 and S100A9 aggravate CVB3-induced myocarditis and might serve as therapeutic targets in inflammatory cardiomyopathies.
Source: Circulation: Heart Failure - November 20, 2017 Category: Cardiology Authors: Muller, I., Vogl, T., Pappritz, K., Miteva, K., Savvatis, K., Rohde, D., Most, P., Lassner, D., Pieske, B., Kuhl, U., Van Linthout, S., Tschope, C. Tags: Animal Models of Human Disease, Basic Science Research, Cardiomyopathy Original Articles Source Type: research

Synergistic effect of HIF ‐1α and FoxO3a trigger cardiomyocyte apoptosis under hyperglycemic ischemia condition
This article is protected by copyright. All rights reserved
Source: Journal of Cellular Physiology - October 14, 2017 Category: Cytology Authors: Ya ‐Fang Chen, Sudhir Pandey, Cecilia Hsuan Day, Yu‐Feng Chen, Ai‐Zhi Jiang, Tsung‐Jung Ho, Ray‐Jade Chen, Vijaya PadmaViswanadha, Wei‐Wen Kuo, Chih‐Yang Huang Tags: ORIGINAL RESEARCH ARTICLE Source Type: research

Spironolactone-induced degradation of the TFIIH core complex XPB subunit suppresses NF- κB and AP-1 signalling
ConclusionSPL has important anti-inflammatory effects independent of aldosterone and MR, not shared with EPL. Drug-induced, proteasome-dependent XPB degradation may be a useful therapeutic approach in cardiovascular diseases driven by inflammation.
Source: Cardiovascular Research - September 27, 2017 Category: Cardiology Source Type: research

Salt-induced Na(+)/K(+)-ATPase- α/β expression involves soluble adenylyl cyclase in endothelial cells.
Salt-induced Na(+)/K(+)-ATPase-α/β expression involves soluble adenylyl cyclase in endothelial cells. Pflugers Arch. 2017 May 26;: Authors: Mewes M, Nedele J, Schelleckes K, Bondareva O, Lenders M, Kusche-Vihrog K, Schnittler HJ, Brand SM, Schmitz B, Brand E Abstract High dietary salt intake may lead to vascular stiffness, which predicts cardiovascular diseases such as heart failure, and myocardial and cerebral infarctions as well as renal impairment. The vascular endothelium is a primary target for deleterious salt effects leading to dysfunction and endothelial stiffness. We hypothesize that the Ca...
Source: Pflugers Archiv : European Journal of Physiology - May 26, 2017 Category: Physiology Authors: Mewes M, Nedele J, Schelleckes K, Bondareva O, Lenders M, Kusche-Vihrog K, Schnittler HJ, Brand SM, Schmitz B, Brand E Tags: Pflugers Arch Source Type: research

Contribution of two pore potassium channels to cardiac ventricular action potential revealed using human iPSC-derived cardiomyocytes.
Abstract Two pore potassium channels (K2p) have been described in modulating background conductance as leak channels in different physiological systems. In the heart, the expression of K2p channels is heterogeneous with equivocation regarding their functional role. Our objective was to determine the K2p expression profile and their physiological and pathophysiological contribution to cardiac electrophysiology. Induced pluripotent stem cells (iPSC) cells generated from humans were differentiated into cardiomyocytes (iPSC-CM). mRNA was isolated from these cells, commercial iPSC-CM (iCells®), control human heart ven...
Source: American Journal of Physiology. Heart and Circulatory Physiology - March 24, 2017 Category: Physiology Authors: Chai S, Wan X, Nassal DM, Liu H, Moravec CS, Ramirez-Navarro A, Deschenes I Tags: Am J Physiol Heart Circ Physiol Source Type: research

Ghrelin protected neonatal rat cardiomyocyte against hypoxia/reoxygenation injury by inhibiting apoptosis through Akt-mTOR signal.
In conclusion, Ghrelin can reduce the H/R damage on NRCMs and inhibit the apoptosis by activating Akt-mTOR signaling pathway. PMID: 28281036 [PubMed - as supplied by publisher]
Source: Molecular Biology Reports - March 8, 2017 Category: Molecular Biology Authors: Wang L, Lu Y, Liu X, Wang X Tags: Mol Biol Rep Source Type: research

Mnk1 (Mitogen-Activated Protein Kinase-Interacting Kinase 1) Deficiency Aggravates Cardiac Remodeling in MiceNovelty and Significance Heart
Identifying the key factor involved in cardiac remodeling is critically important for developing novel strategies to protect against heart failure. Here, the role of Mnk1 (mitogen-activated protein kinase–interacting kinase 1) in cardiac remodeling was clarified. Cardiac remodeling was induced by transverse aortic constriction in Mnk1-knockout mice and their wild-type control mice. After 4 weeks of transverse aortic constriction, Mnk1-knockout mice developed exaggerated cardiac hypertrophy, fibrosis, dysfunction, and cardiomyocyte apoptosis and showed increased ERK1/2 (extracellular signal–regulated kinase 1/2) activat...
Source: Hypertension - November 8, 2016 Category: Cardiology Authors: Yuan, Y., Yan, L., Wu, Q.-Q., Zhou, H., Jin, Y.-G., Bian, Z.-Y., Deng, W., Yang, Z., Shen, D.-F., Zeng, X.-F., Wang, S.-S., Li, H., Tang, Q.-Z. Tags: Hypertrophy, Remodeling Original Articles Source Type: research

PSGR olfactory receptor: A new potential target in pulmonary arterial hypertension
Pulmonary arterial hypertension (PAH) is a rare progressive disease due to distal vascular remodeling, leading to right heart failure and death. PSGR is an olfactory receptor (OR) that has been recently detected in peripheral tissues. Moreover, PSGR overexpression is associated with pro-proliferative phenotype in prostate cancer. Since PAH vascular cells are characterized by cancer-like over-proliferation, we hypothesized that PSGR might participate in the vascular remodeling leading to PAH.Here we aimed to determine whether upregulation of PSGR is implicated in PAH pathological phenotype, and to explore PSGR as a novel th...
Source: European Respiratory Journal - November 7, 2016 Category: Respiratory Medicine Authors: Courboulin, A., Quatredeniers, M., Sanz, G., Breuils-Bonnet, S., Vocelle, M., Lafond, M., Perros, F., Bonnet, S., Pajot-Augy, E., Humbert, M., Cohen-Kaminsky, S. Tags: 4.3 Pulmonary Circulation and Pulmonary Vascular Diseases Source Type: research

Endothelin-1-Induced Cell Hypertrophy in Cardiomyocytes is Improved by Fenofibrate: Possible Roles of Adiponectin.
CONCLUSIONS: Our study shows that fenofibrate may protect against ET-1-induced cardiomyocyte hypertrophy and enhanced adiponectin expression through modulation of PPARα expression in vitro and limitation of daunorubicin cardiotoxicity in vivo, suggesting a novel mechanistic insight into the role of PPARα and adiponectin in cardiac hypertrophy and heart failure. PMID: 27629528 [PubMed - as supplied by publisher]
Source: Journal of Atherosclerosis and Thrombosis - September 19, 2016 Category: Cardiology Tags: J Atheroscler Thromb Source Type: research

NAD(P)H Oxidase 4 Activation via Angiotensin II induces Protein Degradation in Skeletal Myocytes
Background: Skeletal muscle atrophy is observed in aging and a variety of diseases, including chronic kidney disease and heart failure. We have previously reported that angiotensin II (Ang II), a key mediator of the renin-angiotensin system, directly induced skeletal muscle atrophy in mice. Here we hypothesized that the activation of NAD(P)H oxidase 4 (Nox4) by Ang II induces protein degradation in skeletal myocytes. Methods: Mouse skeletal myocytes(C2C12) were cultured. They were transfected by electroporation with Nox4 small interference RNA (siRNA).
Source: Journal of Cardiac Failure - August 24, 2016 Category: Cardiology Authors: Tomoyasu Kadoguchi, Kazunori Shimada, Tomoyuki Shiozawa, Shuhei Takahashi, Hamad Al Shahi, Yuta Komano, Tetsuro Miyazaki, Koji Akita, Kikuo Isoda, Hiroyuki Daida Source Type: research

Phosphocreatine attenuates angiotensin II-induced cardiac fibrosis in rat cardiomyocytes through modulation of MAPK and NF-κB pathway.
CONCLUSIONS: Our study determined that PCr protected cardiomyocytes from Ang II-induced CF through inhibition of MAPK and NF-κB pathway. PMID: 27383329 [PubMed - in process]
Source: European Review for Medical and Pharmacological Sciences - July 9, 2016 Category: Drugs & Pharmacology Tags: Eur Rev Med Pharmacol Sci Source Type: research