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Cardiac Contractility Modulation

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https://www.readbyqxmd.com/read/28275246/sarcoplasmic-reticulum-mitochondria-communication-in-cardiovascular-pathophysiology
#1
REVIEW
Camila Lopez-Crisosto, Christian Pennanen, Cesar Vasquez-Trincado, Pablo E Morales, Roberto Bravo-Sagua, Andrew F G Quest, Mario Chiong, Sergio Lavandero
Repetitive, calcium-mediated contractile activity renders cardiomyocytes critically dependent on a sustained energy supply and adequate calcium buffering, both of which are provided by mitochondria. Moreover, in vascular smooth muscle cells, mitochondrial metabolism modulates cell growth and proliferation, whereas cytosolic calcium levels regulate the arterial vascular tone. Physical and functional communication between mitochondria and sarco/endoplasmic reticulum and balanced mitochondrial dynamics seem to have a critical role for optimal calcium transfer to mitochondria, which is crucial in calcium homeostasis and mitochondrial metabolism in both types of muscle cells...
March 9, 2017: Nature Reviews. Cardiology
https://www.readbyqxmd.com/read/28256297/insulin-and-%C3%AE-adrenergic-receptor-signaling-crosstalk-in-heart
#2
REVIEW
Qin Fu, Qingtong Wang, Yang K Xiang
Recent advances show that insulin may affect β adrenergic receptor (βAR) signaling in the heart to modulate cardiac function in clinically relevant states, such as diabetes mellitus (DM) and heart failure (HF). Conversely, activation of βAR regulates cardiac glucose uptake and promotes insulin resistance (IR) in HF. Here, we discuss the recent characterization of the interaction between the cardiac insulin receptor (InsR) and βAR in the myocardium, in which insulin stimulation crosstalks with cardiac βAR via InsR substrate (IRS)-dependent and G-protein receptor kinase 2 (GRK2)-mediated phosphorylation of β2AR...
February 27, 2017: Trends in Endocrinology and Metabolism: TEM
https://www.readbyqxmd.com/read/28229200/-current-impact-of-cardiac-implantable-electronic-devices
#3
J Kuschyk, B Rudic, M Borggrefe, I Akin
Sudden cardiac death and chronic heart failure are among the main contributors to persisting high mortality rates in Germany. In addition to removal of causal factors and guideline-conform pharmacological therapy, therapy with cardiac implantable electronic devices (CIED) is of undisputed importance. Subcutaneous defibrillators have the advantage that they do not have intracardiac electrodes but still have the same efficacy and safety. For patients with a wide QRS complex and reduced ejection fraction, cardiac resynchronization has led to a reduction of morbidity and mortality...
February 22, 2017: Herz
https://www.readbyqxmd.com/read/28223222/disrupting-the-key-circadian-regulator-clock-leads-to-age-dependent-cardiovascular-disease
#4
Faisal J Alibhai, Jonathan LaMarre, Cristine J Reitz, Elena V Tsimakouridze, Jeffrey T Kroetsch, Steffen-Sebastian Bolz, Alex Shulman, Samantha Steinberg, Thomas P Burris, Gavin Y Oudit, Tami A Martino
The circadian mechanism underlies daily rhythms in cardiovascular physiology and rhythm disruption is a major risk factor for heart disease and worse outcomes. However, the role of circadian rhythms is generally clinically unappreciated. Clock is a core component of the circadian mechanism and here we examine the role of Clock as a vital determinant of cardiac physiology and pathophysiology in aging. Clock(Δ19/Δ19) mice develop age-dependent increases in heart weight, hypertrophy, dilation, impaired contractility, and reduced myogenic responsiveness...
February 20, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28138563/ganglionic-gfap-glial-gq-gpcr-signaling-enhances-heart-functions-in-vivo
#5
Alison Xiaoqiao Xie, Jakovin J Lee, Ken D McCarthy
The sympathetic nervous system (SNS) accelerates heart rate, increases cardiac contractility, and constricts resistance vessels. The activity of SNS efferent nerves is generated by a complex neural network containing neurons and glia. Gq G protein-coupled receptor (Gq-GPCR) signaling in glial fibrillary acidic protein-expressing (GFAP(+)) glia in the central nervous system supports neuronal function and regulates neuronal activity. It is unclear how Gq-GPCR signaling in GFAP(+) glia affects the activity of sympathetic neurons or contributes to SNS-regulated cardiovascular functions...
January 26, 2017: JCI Insight
https://www.readbyqxmd.com/read/28134997/mass-transport-circulatory-system-with-emphasis-on-nonendothermic-species
#6
Dane A Crossley, Warren W Burggren, Carl L Reiber, Jordi Altimiras, Kenneth J Rodnick
Mass transport can be generally defined as movement of material matter. The circulatory system then is a biological example given its role in the movement in transporting gases, nutrients, wastes, and chemical signals. Comparative physiology has a long history of providing new insights and advancing our understanding of circulatory mass transport across a wide array of circulatory systems. Here we focus on circulatory function of nonmodel species. Invertebrates possess diverse convection systems; that at the most complex generate pressures and perform at a level comparable to vertebrates...
December 6, 2016: Comprehensive Physiology
https://www.readbyqxmd.com/read/28116799/in-vitro-models-of-the-cardiac-microenvironment-to-study-myocyte-and-non-myocyte-crosstalk-bioinspired-approaches-beyond-the-polystyrene-dish
#7
Celinda M Kofron, Ulrike Mende
The heart is a complex pluricellular organ composed of cardiomyocytes and non-myocytes including fibroblasts, endothelial cells and immune cells. Myocytes are responsible for electrical conduction and contractile force generation, while the other cell types are responsible for matrix deposition, vascularization, and injury response. Myocytes and non-myocytes are known to communicate and exert mutual regulatory effects. In concert, they determine the structural, electrical and mechanical characteristics in the healthy and remodelled myocardium...
January 23, 2017: Journal of Physiology
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
#8
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
#9
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
#10
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
#11
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
#12
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
#13
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
#14
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)...
January 31, 2017: Oncotarget
https://www.readbyqxmd.com/read/27994552/exercise-training-attenuates-right-ventricular-remodeling-in-rats-with-pulmonary-arterial-stenosis
#15
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-receptor-signaling
#16
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 types of 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...
February 3, 2017: 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
#17
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
#18
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
#19
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
#20
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
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