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Cardiac Contractility Modulation

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https://www.readbyqxmd.com/read/28101624/the-safety-and-efficacy-of-cardiac-contractility-modulation-in-heart-failure-a%C3%A2-meta-analysis-of-clinical-trials
#1
X Liu, H J Yang, H Q Ping, S Qiu, S Shi, B Yang
BACKGROUND: Cardiac contractility modulation (CCM) has developed as a promising treatment device for heart failure (HF). This meta-analysis aimed at systematically reviewing the latest available published trials to provide evidence on the safety and efficacy of CCM in patients with HF. METHODS: We searched the Cochrane Central Resister of Controlled Trials, PubMed, and EMBASE in May 2016 to identify eligible clinical trials comparing CCM with sham treatment or with usual care...
January 18, 2017: Herz
https://www.readbyqxmd.com/read/28101410/modulation-of-cardiomyocyte-activity-using-pulsed-laser-irradiated-gold-nanoparticles
#2
Lara Gentemann, Stefan Kalies, Michelle Coffee, Heiko Meyer, Tammo Ripken, Alexander Heisterkamp, Robert Zweigerdt, Dag Heinemann
Can photothermal gold nanoparticle mediated laser manipulation be applied to induce cardiac contraction? Based on our previous work, we present a novel concept of cell stimulation. A 532 nm picosecond laser was employed to heat gold nanoparticles on cardiomyocytes. This leads to calcium oscillations in the HL-1 cardiomyocyte cell line. As calcium is connected to the contractility, we aimed to alter the contraction rate of native and stem cell derived cardiomyocytes. A contraction rate increase was particularly observed in calcium containing buffer with neonatal rat cardiomyocytes...
January 1, 2017: Biomedical Optics Express
https://www.readbyqxmd.com/read/28098356/mechano-chemo-transduction-in-cardiac-myocytes
#3
Ye Chen-Izu, Leighton T Izu
The heart has the ability to adjust to changing mechanical loads. The Frank-Starling law and the Anrep effect describe exquisite intrinsic mechanisms the heart has for autoregulating the force of contraction to maintain cardiac output under preload and afterload. Although these mechanisms have been known for more than a century, their cellular and molecular underpinnings are still debated. How does the cardiac myocyte sense a change in preload or afterload? How does the myocyte adjust its response to compensate for such changes? In cardiac myocytes Ca(2+) is a crucial regulator of contractile force and in this review we compare and contrast recent results from different labs that address two important questions...
January 18, 2017: Journal of Physiology
https://www.readbyqxmd.com/read/28096047/cellular-basis-of-angiotensin-1-7-induced-augmentation-of-left-ventricular-functional-performance-in-heart-failure
#4
Xiaowei Zhang, Heng-Jie Cheng, Peng Zhou, Dalane W Kitzman, Carlos M Ferrario, Wei-Min Li, Che Ping Cheng
BACKGROUND: Angiotensin-(1-7) [Ang-(1-7)] exhibits cardiovascular effects opposite those of angiotensin II (Ang II), thus providing protection against heart disease. However, how Ang-(1-7) imparts cardioprotection is unclear, and its direct cardiac effects are controversial. Whether heart failure (HF) alters cardiac contractile responses to Ang-(1-7) remains undetermined. We tested the hypothesis that in HF, Ang-(1-7) may produce positive modulation on [Ca(2+)]i regulation, enhancing left ventricular (LV) and myocyte contraction and relaxation via Ang-(1-7) Mas receptor coupled with nitric oxide (NO)/bradykinin (BK)-mediated mechanism...
January 10, 2017: International Journal of Cardiology
https://www.readbyqxmd.com/read/28069793/decreased-wnt-%C3%AE-catenin-signalling-contributes-to-the-pathogenesis-of-dilated-cardiomyopathy-caused-by-mutations-in-the-lamin-a-c-gene
#5
Caroline Le Dour, Coline Macquart, Fusako Sera, Shunichi Homma, Gisele Bonne, John P Morrow, Howard J Worman, Antoine Muchir
Cardiomyopathy caused by lamin A/C gene (LMNA) mutations (hereafter referred as LMNA cardiomyopathy) is characterized by cardiac conduction abnormalities and left ventricular systolic dysfunction predisposing to heart failure. Previous cardiac transcriptional profiling of Lmna(H222P/H222P) mouse, a small animal model of LMNA cardiomyopathy, suggested decreased WNT/β-catenin signalling. We confirmed decreased WNT/β-catenin signalling in the hearts of these mice by demonstrating decreased β-catenin and WNT proteins...
January 9, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/28045017/protective-effects-of-intercalated-disk-protein-afadin-on-chronic-pressure-overload-induced-myocardial-damage
#6
Dimitar P Zankov, Akio Shimizu, Miki Tanaka-Okamoto, Jun Miyoshi, Hisakazu Ogita
Adhesive intercellular connections at cardiomyocyte intercalated disks (IDs) support contractile force and maintain structural integrity of the heart muscle. Disturbances of the proteins at IDs deteriorate cardiac function and morphology. An adaptor protein afadin, one of the components of adherens junctions, is expressed ubiquitously including IDs. At present, the precise role of afadin in cardiac physiology or disease is unknown. To explore this, we generated conditional knockout (cKO) mice with cardiomyocyte-targeted deletion of afadin...
January 3, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28039445/aromatase-inhibitor-induced-bone-loss-increases-the-progression-of-estrogen-receptor-negative-breast-cancer-in-bone-and-exacerbates-muscle-weakness-in-vivo
#7
Laura E Wright, Ahmed A Harhash, Wende M Kozlow, David L Waning, Jenna N Regan, Yun She, Sutha K John, Sreemala Murthy, Maryla Niewolna, Andrew R Marks, Khalid S Mohammad, Theresa A Guise
Aromatase inhibitors (AIs) cause muscle weakness, bone loss, and joint pain in up to half of cancer patients. Preclinical studies have demonstrated that increased osteoclastic bone resorption can impair muscle contractility and prime the bone microenvironment to accelerate metastatic growth. We hypothesized that AI-induced bone loss could increase breast cancer progression in bone and exacerbate muscle weakness associated with bone metastases. Female athymic nude mice underwent ovariectomy (OVX) or sham surgery and were treated with vehicle or AI (letrozole; Let)...
December 25, 2016: Oncotarget
https://www.readbyqxmd.com/read/27994552/exercise-training-attenuates-right-ventricular-remodeling-in-rats-with-pulmonary-arterial-stenosis
#8
Brunno Lemes de Melo, Stella S Vieira, Ednei L Antônio, Luís F N Dos Santos, Leslie A Portes, Regiane S Feliciano, Helenita A de Oliveira, José A Silva, Paulo de Tarso C de Carvalho, Paulo J F Tucci, Andrey J Serra
Introduction: Pulmonary arterial stenosis (PAS) is a congenital defect that causes outflow tract obstruction of the right ventricle (RV). Currently, negative issues are reported in the PAS management: not all patients may be eligible to surgeries; there is often the need for another surgery during passage to adulthood; patients with mild stenosis may have later cardiac adverse repercussions. Thus, the search for approaches to counteract the long-term PAS effects showed to be a current target. At the study herein, we evaluated the cardioprotective role of exercise training in rats submitted to PAS for 9 weeks...
2016: Frontiers in Physiology
https://www.readbyqxmd.com/read/27994053/apelin-36-modulates-blood-glucose-and-body-weight-independently-of-canonical-apj-signaling
#9
Hadas Galon-Tilleman, Hong Yang, Maria A Bednarek, Sandra M Spurlock, Kevin J Paavola, Brian Ko, Carmen To, Jian Luo, Hui Tian, Lutz Jermutus, Joseph Grimsby, Cristina M Rondinone, Anish Konkar, Daniel D Kaplan
Apelin-36 was discovered as the endogenous ligand for the previously orphan receptor APJ. Apelin-36 has been linked to two major biological activities - cardiovascular (stimulation of cardiac contractility and suppression of blood pressure) and metabolic (improving glucose homeostasis and lowering body weight). It has been assumed that both of these activities are modulated through APJ. Here, we demonstrate that the metabolic activity of apelin-36 can be separated from canonical APJ activation. We developed a series of apelin-36 variants in which evolutionarily conserved residues were mutated, and evaluated their ability to modulate glucose homeostasis and body weight in chronic mouse models...
December 19, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/27975185/l71f-mutation-in-rat-cardiac-troponin-t-augments-crossbridge-recruitment-and-detachment-dynamics-against-%C3%AE-myosin-heavy-chain-but-not-against-%C3%AE-myosin-heavy-chain
#10
Sherif M Reda, Sampath K Gollapudi, Murali Chandra
The N-terminal extension of human cardiac troponin T (TnT), which modulates myofilament Ca(2+) sensitivity, contains several hypertrophic cardiomyopathy (HCM)-causing mutations including S69F. However, the functional consequence of S69F mutation is unknown. The human analog of S69F in rat TnT is L71F (TnTL71F). Because the functional consequences due to structural changes in the N-terminal extension are influenced by the type of myosin heavy chain (MHC) isoform, we hypothesized that the TnTL71F-mediated effect would be differently modulated by α- and β-MHC isoforms...
December 14, 2016: Journal of Muscle Research and Cell Motility
https://www.readbyqxmd.com/read/27930744/interactions-of-calcium-fluctuations-during-cardiomyocyte-contraction-with-real-time-camp-dynamics-detected-by-fret
#11
Julia U Sprenger, Nadja I Bork, Jonas Herting, Thomas H Fischer, Viacheslav O Nikolaev
Calcium (Ca2+) and 3',5'-cyclic adenosine monophosphate (cAMP) play a critical role for cardiac excitation-contraction-coupling. Both second messengers are known to interact with each other, for example via Ca2+-dependent modulation of phosphodiesterase 1 (PDE1) and adenylyl cyclase 5/6 (AC 5/6) activities, which is supposed to occur especially at the local level in distinct subcellular microdomains. Currently, many studies analyze global and local cAMP signaling and its regulation in resting cardiomyocytes devoid of electrical stimulation...
2016: PloS One
https://www.readbyqxmd.com/read/27895893/downregulation-of-long-non-coding-rna-h19-promotes-p19cl6-cells-proliferation-and-inhibits-apoptosis-during-late-stage-cardiac-differentiation-via-mir-19b-modulated-sox6
#12
Yu Han, Hongdang Xu, Jiangtao Cheng, Yanwei Zhang, Chuanyu Gao, Taibing Fan, Bangtian Peng, Bin Li, Lin Liu, Zhaoyun Cheng
BACKGROUND: Regulating cardiac differentiation to maintain normal heart development and function is very important. At present, biological functions of H19 in cardiac differentiation is not completely clear. METHODS: To explore the functional effect of H19 during cardiac differentiation. Expression levels of early cardiac-specific markers Nkx-2.5 and GATA4, cardiac contractile protein genes α-MHC and MLC-2v were determined by qRT-PCR and western lot. The levels of lncRNA H19 and miR-19b were detected by qRT-PCR...
2016: Cell & Bioscience
https://www.readbyqxmd.com/read/27886226/functional-improvement-and-regression-of-medial-hypertrophy-in-the-remodeled-pulmonary-artery-after-correction-of-systemic-left-to-right-shunt
#13
Chih-Hsin Hsu, Jun-Neng Roan, Jyh-Hong Chen, Chen-Fuh Lam
The presence of systemic left-to-right shunt and increased pulmonary blood flow can result in right heart failure and pulmonary arteriopathy. Correction of left-to-right shunt has been shown to improve cardiac function and physical performance. However, the cardiopulmonary remodeling processes following cessation of left-to-right shunt have yet to be reported. In this experimental study, excessive pulmonary flow was restored through ligation of the aortocaval fistula in rats with flow-induced pulmonary hypertension...
November 25, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27880847/activation-of-both-the-calpain-and-ubiquitin-proteasome-systems-contributes-to-septic-cardiomyopathy-through-dystrophin-loss-disruption-and-mtor-inhibition
#14
Ana Caroline Silva Freitas, Maria Jose Figueiredo, Erica Carolina Campos, Danilo Figueiredo Soave, Simone Gusmao Ramos, Herbert B Tanowitz, Mara Rúbia N Celes
Cardiac dysfunction caused by the impairment of myocardial contractility has been recognized as an important factor contributing to the high mortality in sepsis. Calpain activation in the heart takes place in response to increased intracellular calcium influx resulting in proteolysis of structural and contractile proteins with subsequent myocardial dysfunction. The purpose of the present study was to test the hypothesis that increased levels of calpain in the septic heart leads to disruption of structural and contractile proteins and that administration of calpain inhibitor-1 (N-acetyl-leucinyl-leucinyl-norleucinal (ALLN)) after sepsis induced by cecal ligation and puncture prevents cardiac protein degradation...
2016: PloS One
https://www.readbyqxmd.com/read/27867086/diazoxide-prevents-reactive-oxygen-species-and-mitochondrial-damage-leading-to-anti-hypertrophic-effects
#15
Aline M Lucas, Francisco R Caldas, Amanda P da Silva, Maximiano M Ventura, Iago M Leite, Ana B Filgueiras, Claúdio G L Silva, Alicia J Kowaltowski, Heberty T Facundo
Pathological cardiac hypertrophy is characterized by wall thickening or chamber enlargement of the heart in response to pressure or volume overload, respectively. This condition will, initially, improve the organ contractile function, but if sustained will render dysfunctional mitochondria and oxidative stress. Mitochondrial ATP-sensitive K(+) channels (mitoKATP) modulate the redox status of the cell and protect against several cardiac insults. Here, we tested the hypothesis that mitoKATP opening (using diazoxide) will avoid isoproterenol-induced cardiac hypertrophy in vivo by decreasing reactive oxygen species (ROS) production and mitochondrial Ca(2+)-induced swelling...
January 5, 2017: Chemico-biological Interactions
https://www.readbyqxmd.com/read/27845246/palmitate-promotes-inflammatory-responses-and-cellular-senescence-in-cardiac-fibroblasts
#16
Marina Sokolova, Leif Erik Vinge, Katrine Alfsnes, Maria Belland Olsen, Lars Eide, Ole Jørgen Kaasbøll, Håvard Attramadal, May-Kristin Torp, Linn E Fosshaug, Azita Rashidi, Egil Lien, Alexandra Vanessa Finsen, Øystein Sandanger, Pål Aukrust, Trine Ranheim, Arne Yndestad
Palmitate triggers inflammatory responses in several cell types, but its effects on cardiac fibroblasts are at present unknown. The aims of the study were to (1) assess the potential of palmitate to promote inflammatory signaling in cardiac fibroblasts through TLR4 and the NLRP3 inflammasome and (2) characterize the cellular phenotype of cardiac fibroblasts exposed to palmitate. We examined whether palmitate induces inflammatory responses in cardiac fibroblasts from WT, NLRP3(-/-) and ASC(-/-)mice (C57BL/6 background)...
February 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/27844333/cardiac-autonomic-innervation
#17
Hina K Jamali, Fahad Waqar, Myron C Gerson
The autonomic nervous system plays a key role in regulating changes in the cardiovascular system and its adaptation to various human body functions. The sympathetic arm of the autonomic nervous system is associated with the fight and flight response, while the parasympathetic division is responsible for the restorative effects on heart rate, blood pressure, and contractility. Disorders involving these two divisions can lead to, and are seen as, a manifestation of most common cardiovascular disorders. Over the last few decades, extensive research has been performed establishing imaging techniques to quantify the autonomic dysfunction associated with various cardiovascular disorders...
November 14, 2016: Journal of Nuclear Cardiology: Official Publication of the American Society of Nuclear Cardiology
https://www.readbyqxmd.com/read/27837311/17%C3%AE-estradiol-induced-interaction-of-estrogen-receptor-%C3%AE-and-human-atrial-essential-myosin-light-chain-modulates-cardiac-contractile-function
#18
Karolin Duft, Miriam Schanz, Hang Pham, Ahmed Abdelwahab, Cindy Schriever, Georgios Kararigas, Elke Dworatzek, Mercy M Davidson, Vera Regitz-Zagrosek, Ingo Morano, Shokoufeh Mahmoodzadeh
Chronic increased workload of the human heart causes ventricular hypertrophy, re-expression of the atrial essential myosin light chain (hALC-1), and improved contractile function. Although hALC-1 is an important positive inotropic regulator of the human heart, little is known about its regulation. Therefore, we investigated the role of the sex hormone 17β-estradiol (E2) on hALC-1 gene expression, the underlying molecular mechanisms, and the impact of this regulatory process on cardiac contractile function...
January 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/27825850/the-role-of-%C3%AE-smooth-muscle-actin-in-fibroblast-mediated-matrix-contraction-and-remodeling
#19
Arti V Shinde, Claudio Humeres, Nikolaos G Frangogiannis
Cardiac myofibroblasts play an important role in myocardial remodeling. Although α-smooth muscle actin (α-SMA) expression is the hallmark of mature myofibroblasts, its role in regulating fibroblast function remains poorly understood. We explore the effects of the matrix environment in modulating cardiac fibroblast phenotype, and we investigate the role of α-SMA in fibroblast function using loss- and gain-of-function approaches. In murine myocardial infarction, infiltration of the infarct border zone with abundant α-SMA-positive myofibroblasts was associated with scar contraction...
January 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/27825670/left-atrial-volume-and-function-in-dogs-with-naturally-occurring-myxomatous-mitral-valve-disease
#20
M Höllmer, J L Willesen, A Tolver, J Koch
OBJECTIVE: Myxomatous mitral valve disease (MMVD) induces progressive left atrial (LA) enlargement. The LA modulates left ventricular filling and performance through its reservoir, conduit, and contractile function. Assessment of LA size and function may provide valuable information on the level of cardiac compensation. Left atrial function in dogs with naturally occurring MMVD remains largely unexplored. The objective of this study was to evaluate LA volume and function in dogs with naturally occurring MMVD...
November 5, 2016: Journal of Veterinary Cardiology: the Official Journal of the European Society of Veterinary Cardiology
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