Platelet inhibitors influence cardioprotection: importance in preclinical study design: reply
(Source: Cardiovascular Research)
Source: Cardiovascular Research - March 17, 2015 Category: Cardiology Authors: Lecour, S., Schulz, R., Ferdinandy, P., Hausenloy, D. J. Tags: LETTERS TO THE EDITOR Source Type: research

Status of P2Y12 treatment must be considered in evaluation of myocardial ischaemia/reperfusion injury
(Source: Cardiovascular Research)
Source: Cardiovascular Research - March 17, 2015 Category: Cardiology Authors: Cohen, M. V., Downey, J. M. Tags: LETTERS TO THE EDITOR Source Type: research

Reconciling computer models and stem cell models of human cardiac repolarization: reply
(Source: Cardiovascular Research)
Source: Cardiovascular Research - March 17, 2015 Category: Cardiology Authors: Han, L., Li, Y., Tchao, J., Kaplan, A. D., Lin, B., Li, Y., Mich-Basso, J., Lis, A., Hassan, N., London, B., Bett, G. C. L., Tobita, K., Rasmusson, R. L., Yang, L. Tags: LETTERS TO THE EDITOR Source Type: research

Prolonged action potentials in HCM-derived iPSC - biology or artefact?
(Source: Cardiovascular Research)
Source: Cardiovascular Research - March 17, 2015 Category: Cardiology Authors: Christ, T., Koivumaki, J. T., Eschenhagen, T. Tags: LETTERS TO THE EDITOR Source Type: research

Some 'brain' in the heart: a novel microdomain with neuronal Na channels responsible for arrhythmias?
(Source: Cardiovascular Research)
Source: Cardiovascular Research - March 17, 2015 Category: Cardiology Authors: Maier, L. S. Tags: EDITORIALS Source Type: research

Cardiac Fgf21 synthesis and release: an autocrine loop for boosting up antioxidant defenses in failing hearts
(Source: Cardiovascular Research)
Source: Cardiovascular Research - March 17, 2015 Category: Cardiology Authors: Di Lisa, F., Itoh, N. Tags: EDITORIALS Source Type: research

Contents Page
(Source: Cardiovascular Research)
Source: Cardiovascular Research - March 17, 2015 Category: Cardiology Tags: FRONT-MATTER/BACK-MATTER Source Type: research

Aims and Scope
(Source: Cardiovascular Research)
Source: Cardiovascular Research - March 17, 2015 Category: Cardiology Tags: FRONT-MATTER/BACK-MATTER Source Type: research

Editorial Board
(Source: Cardiovascular Research)
Source: Cardiovascular Research - March 17, 2015 Category: Cardiology Tags: FRONT-MATTER/BACK-MATTER Source Type: research

Cover Page
(Source: Cardiovascular Research)
Source: Cardiovascular Research - March 17, 2015 Category: Cardiology Tags: FRONT-MATTER/BACK-MATTER Source Type: research

Targets for therapy in sarcomeric cardiomyopathies
To date, no compounds or interventions exist that treat or prevent sarcomeric cardiomyopathies. Established therapies currently improve the outcome, but novel therapies may be able to more fundamentally affect the disease process and course. Investigations of the pathomechanisms are generating molecular insights that can be useful for the design of novel specific drugs suitable for clinical use. As perturbations in the heart are stage-specific, proper timing of drug treatment is essential to prevent initiation and progression of cardiac disease in mutation carrier individuals. In this review, we emphasize potential novel t...
Source: Cardiovascular Research - March 4, 2015 Category: Cardiology Authors: Tardiff, J. C., Carrier, L., Bers, D. M., Poggesi, C., Ferrantini, C., Coppini, R., Maier, L. S., Ashrafian, H., Huke, S., van der Velden, J. Tags: INVITED SPOTLIGHT REVIEWS Source Type: research

Research priorities in sarcomeric cardiomyopathies
The clinical variability in patients with sarcomeric cardiomyopathies is striking: a mutation causes cardiomyopathy in one individual, while the identical mutation is harmless in a family member. Moreover, the clinical phenotype varies ranging from asymmetric hypertrophy to severe dilatation of the heart. Identification of a single phenotype-associated disease mechanism would facilitate the design of targeted treatments for patient groups with different clinical phenotypes. However, evidence from both the clinic and basic knowledge of functional and structural properties of the sarcomere argues against a ‘one size fi...
Source: Cardiovascular Research - March 4, 2015 Category: Cardiology Authors: van der Velden, J., Ho, C. Y., Tardiff, J. C., Olivotto, I., Knollmann, B. C., Carrier, L. Tags: INVITED SPOTLIGHT REVIEWS Source Type: research

Animal and in silico models for the study of sarcomeric cardiomyopathies
Over the past decade, our understanding of cardiomyopathies has improved dramatically, due to improvements in screening and detection of gene defects in the human genome as well as a variety of novel animal models (mouse, zebrafish, and drosophila) and in silico computational models. These novel experimental tools have created a platform that is highly complementary to the naturally occurring cardiomyopathies in cats and dogs that had been available for some time. A fully integrative approach, which incorporates all these modalities, is likely required for significant steps forward in understanding the molecular underpinni...
Source: Cardiovascular Research - March 4, 2015 Category: Cardiology Authors: Duncker, D. J., Bakkers, J., Brundel, B. J., Robbins, J., Tardiff, J. C., Carrier, L. Tags: INVITED SPOTLIGHT REVIEWS Source Type: research

Modelling sarcomeric cardiomyopathies in the dish: from human heart samples to iPSC cardiomyocytes
This article summarizes what is known about the ‘human cardiomyopathy or heart failure phenotype in vitro’, which constitutes the reference for modelling sarcomeric cardiomyopathies in hiPSC-derived cardiomyocytes. The current techniques for hiPSC generation and cardiac myocyte differentiation are briefly reviewed and the few published reports of hiPSC models of sarcomeric cardiomyopathies described. A discussion of promises and challenges of hiPSC-modelling of sarcomeric cardiomyopathies and individualized approaches is followed by a number of questions that, in the view of the authors, need to be answered bef...
Source: Cardiovascular Research - March 4, 2015 Category: Cardiology Authors: Eschenhagen, T., Mummery, C., Knollmann, B. C. Tags: INVITED SPOTLIGHT REVIEWS Source Type: research

Defining phenotypes and disease progression in sarcomeric cardiomyopathies: contemporary role of clinical investigations
Mutations in cardiac sarcomere protein genes are associated with a variety of clinical phenotypes, including hypertrophic (HCM), dilated (DCM), and restrictive (RCM) cardiomyopathy as well as left ventricular non-compaction, with the overlap of morpho-functional manifestations in individual patients and families. Over time, initial phenotypes may undergo profound changes which determine clinical course and disease progression. Although genetic defects causing HCM and DCM have opposite effects at the myofilament level, a number of downstream maladaptive mechanisms, ranging from microvascular dysfunction and ischaemia to myo...
Source: Cardiovascular Research - March 4, 2015 Category: Cardiology Authors: Olivotto, I., d'Amati, G., Basso, C., Van Rossum, A., Patten, M., Emdin, M., Pinto, Y., Tomberli, B., Camici, P. G., Michels, M. Tags: INVITED SPOTLIGHT REVIEWS Source Type: research

Genetic advances in sarcomeric cardiomyopathies: state of the art
Genetic studies in the 1980s and 1990s led to landmark discoveries that sarcomere mutations cause both hypertrophic and dilated cardiomyopathies. Sarcomere mutations also likely play a role in more complex phenotypes and overlap cardiomyopathies with features of hypertrophy, dilation, diastolic abnormalities, and non-compaction. Identification of the genetic cause of these important conditions provides unique opportunities to interrogate and characterize disease pathogenesis and pathophysiology, starting from the molecular level and expanding from there. With such insights, there is potential for clinical translation that ...
Source: Cardiovascular Research - March 4, 2015 Category: Cardiology Authors: Ho, C. Y., Charron, P., Richard, P., Girolami, F., Van Spaendonck-Zwarts, K. Y., Pinto, Y. Tags: INVITED SPOTLIGHT REVIEWS Source Type: research

Sarcomeric cardiomyopathies: from bedside to bench and back
(Source: Cardiovascular Research)
Source: Cardiovascular Research - March 4, 2015 Category: Cardiology Authors: Hasenfuss, G. Tags: EDITORIAL Source Type: research

Contents Page
(Source: Cardiovascular Research)
Source: Cardiovascular Research - March 4, 2015 Category: Cardiology Tags: FRONT-MATTER/BACK-MATTER Source Type: research

Editorial Board
(Source: Cardiovascular Research)
Source: Cardiovascular Research - March 4, 2015 Category: Cardiology Tags: FRONT-MATTER/BACK-MATTER Source Type: research

Cover Page
(Source: Cardiovascular Research)
Source: Cardiovascular Research - March 4, 2015 Category: Cardiology Tags: FRONT-MATTER/BACK-MATTER Source Type: research

Aims and Scope
(Source: Cardiovascular Research)
Source: Cardiovascular Research - March 4, 2015 Category: Cardiology Tags: FRONT-MATTER/BACK-MATTER Source Type: research

A secreted protein (Canopy 2, CNPY2) enhances angiogenesis and promotes smooth muscle cell migration and proliferation
Conclusions CNPY2 is a HIF-1α-regulated, secreted angiogenic growth factor that promotes SMC migration, proliferation, and tissue revascularization. This new target may have a broader profile than currently available proteins. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 23, 2015 Category: Cardiology Authors: Guo, J., Zhang, Y., Mihic, A., Li, S.-H., Sun, Z., Shao, Z., Wu, J., Weisel, R. D., Li, R.-K. Tags: Vascular biology Source Type: research

Reduction of mouse atherosclerosis by urokinase inhibition or with a limited-spectrum matrix metalloproteinase inhibitor
Aims Elevated activity of urokinase plasminogen activator (uPA) and MMPs in human arteries is associated with accelerated atherosclerosis, aneurysms, and plaque rupture. We used Apoe-null mice with macrophage-specific uPA overexpression (SR-uPA mice; a well-characterized model of protease-accelerated atherosclerosis) to investigate whether systemic inhibition of proteolytic activity of uPA or a subset of MMPs can reduce protease-induced atherosclerosis and aortic dilation. Methods and results SR-uPA mice were fed a high-fat diet for 10 weeks and treated either with an antibody inhibiting mouse uPA (mU1) or a control antib...
Source: Cardiovascular Research - February 23, 2015 Category: Cardiology Authors: Hu, J. H., Touch, P., Zhang, J., Wei, H., Liu, S., Lund, I. K., Hoyer-Hansen, G., Dichek, D. A. Tags: Vascular biology Source Type: research

Role of Hic-5 in the formation of microvilli-like structures and the monocyte-endothelial interaction that accelerates atherosclerosis
Conclusion Hic-5 in ECs plays an important role in the formation of microvilli-like structures and in the interaction between ECs and monocytes, leading to monocyte recruitment and subsequent development of atherosclerosis. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 23, 2015 Category: Cardiology Authors: Arita-Okubo, S., Kim-Kaneyama, J.-r., Lei, X.-F., Fu, W.-G., Ohnishi, K., Takeya, M., Miyauchi, A., Honda, H., Itabe, H., Miyazaki, T., Miyazaki, A. Tags: Vascular biology Source Type: research

Essential role for TMEM100 in vascular integrity but limited contributions to the pathogenesis of hereditary haemorrhagic telangiectasia
Conclusion These results demonstrate that TMEM100 has essential functions for the maintenance of vascular integrity as well as the formation of blood vessels. Our results also indicate that down-regulation of Tmem100 is not the central mechanism of HHT pathogenesis, but it may contribute to the development of vascular pathology of HHT by weakening vascular integrity. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 23, 2015 Category: Cardiology Authors: Moon, E.-H., Kim, Y. S., Seo, J., Lee, S., Lee, Y. J., Oh, S. P. Tags: Vascular biology Source Type: research

miR-21-3p regulates cardiac hypertrophic response by targeting histone deacetylase-8
Conclusion Our data reveal a role of miR-21-3p in regulating HDAC8 expression and Akt/Gsk3β pathway, and suggest that modulation of miR-21-3p levels may provide a therapeutic approach for cardiac hypertrophy. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 23, 2015 Category: Cardiology Authors: Yan, M., Chen, C., Gong, W., Yin, Z., Zhou, L., Chaugai, S., Wang, D. W. Tags: Cardiac biology and remodelling Source Type: research

Enhanced {beta}-adrenergic cardiac reserve in Trpm4-/- mice with ischaemic heart failure
Conclusion Deletion of the Trpm4 gene in mice improved survival and significantly enhanced β-adrenergic cardiac reserve after inducing ischaemic HF. This suggests that pharmacological or genetic down-regulation of TRPM4 function might be a novel strategy in the management of HF. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 23, 2015 Category: Cardiology Authors: Jacobs, G., Oosterlinck, W., Dresselaers, T., Geenens, R., Kerselaers, S., Himmelreich, U., Herijgers, P., Vennekens, R. Tags: Cardiac biology and remodelling Source Type: research

TNF-{alpha} down-regulates sarcoplasmic reticulum Ca2+ ATPase expression and leads to left ventricular diastolic dysfunction through binding of NF-{kappa}B to promoter response element
Conclusions TNF-α suppresses SERCA2a gene expression via the IKK/IB/NF-B pathway and binding of NF-B to the SERCA2a gene promoter, and its effect is blocked by simvastatin, demonstrating the potential therapeutic effect of statins in treating inflammation-related diastolic dysfunction. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 23, 2015 Category: Cardiology Authors: Tsai, C.-T., Wu, C.-K., Lee, J.-K., Chang, S.-N., Kuo, Y.-M., Wang, Y.-C., Lai, L.-P., Chiang, F.-T., Hwang, J.-J., Lin, J.-L. Tags: Cardiac biology and remodelling Source Type: research

Cardiomyocyte-specific expression of CYP2J2 prevents development of cardiac remodelling induced by angiotensin II
Conclusion Cardiomyocyte-specific expression of CYP2J2 or treatment with EETs protects against cardiac remodelling by attenuating oxidative stress-mediated NF-Bp65 nuclear translocation via PPAR- activation. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 23, 2015 Category: Cardiology Authors: He, Z., Zhang, X., Chen, C., Wen, Z., Hoopes, S. L., Zeldin, D. C., Wang, D. W. Tags: Cardiac biology and remodelling Source Type: research

PI3K{alpha} is essential for the recovery from Cre/tamoxifen cardiotoxicity and in myocardial insulin signalling but is not required for normal myocardial contractility in the adult heart
Conclusion Our results show that PI3Kα does not directly regulate myocardial contractility, but is required for recovery from tamoxifen/Cre toxicity. The important role for PI3Kα in insulin signalling and recovery from tamoxifen/Cre toxicity justifies caution when using PI3Kα inhibitors in combination with other cardiovascular comorbidities and cardiotoxic compounds in cancer patients. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 23, 2015 Category: Cardiology Authors: McLean, B. A., Zhabyeyev, P., Patel, V. B., Basu, R., Parajuli, N., DesAulniers, J., Murray, A. G., Kassiri, Z., Vanhaesebroeck, B., Oudit, G. Y. Tags: Cardiac biology and remodelling Source Type: research

Epigenetic balance of aberrant Rasal1 promoter methylation and hydroxymethylation regulates cardiac fibrosis
Conclusion Our study provides proof-in-principle evidence that transcriptional suppression of RASAL1 through aberrant promoter methylation contributes to EndMT and ultimately to progression of cardiac fibrosis. Such aberrant methylation can be reversed through Tet3-mediated hydroxymethylation, which can be specifically induced by BMP7. This may reflect a new treatment strategy to stop cardiac fibrosis. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 23, 2015 Category: Cardiology Authors: Xu, X., Tan, X., Tampe, B., Nyamsuren, G., Liu, X., Maier, L. S., Sossalla, S., Kalluri, R., Zeisberg, M., Hasenfuss, G., Zeisberg, E. M. Tags: Cardiac biology and remodelling Source Type: research

Extracardiac control of embryonic cardiomyocyte proliferation and ventricular wall expansion
Conclusions Our results demonstrate that ventricular wall cardiomyocyte proliferation is subdivided into distinct regulatory phases. Each involves instructive cues that originate outside the heart and thereby act on the epicardium in an endocrine manner, a mode of regulation that is mostly unknown in embryogenesis. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 23, 2015 Category: Cardiology Authors: Shen, H., Cavallero, S., Estrada, K. D., Sandovici, I., Kumar, S. R., Makita, T., Lien, C.-L., Constancia, M., Sucov, H. M. Tags: Cardiac biology and remodelling Source Type: research

Functional crosstalk between cardiac fibroblasts and adult cardiomyocytes by soluble mediators
Conclusions Fibroblasts have different roles during physiology and disease in regulating myocardial function via soluble mediators. A crosstalk between fibroblasts and cardiomyocytes, controlled by TGF-β, is crucial in this interaction. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 23, 2015 Category: Cardiology Authors: Cartledge, J. E., Kane, C., Dias, P., Tesfom, M., Clarke, L., Mckee, B., Al Ayoubi, S., Chester, A., Yacoub, M. H., Camelliti, P., Terracciano, C. M. Tags: Cardiac biology and remodelling Source Type: research

Emergence of Orai3 activity during cardiac hypertrophy
Conclusion Cardiac Orai3 is the essential partner of STIM1 and drives voltage-independent Ca2+ entries in adult cardiomyocytes. Arachidonic acid-activated currents, which are supported by Orai3, are present in adult cardiomyocytes and increased during hypertrophy. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 23, 2015 Category: Cardiology Authors: Saliba, Y., Keck, M., Marchand, A., Atassi, F., Ouille, A., Cazorla, O., Trebak, M., Pavoine, C., Lacampagne, A., Hulot, J.-S., Fares, N., Fauconnier, J., Lompre, A.-M. Tags: Cardiac biology and remodelling Source Type: research

Atrial fibrillation: effects beyond the atrium?
Atrial fibrillation (AF) is the most common sustained clinical arrhythmia and is associated with significant morbidity, mostly secondary to heart failure and stroke, and an estimated two-fold increase in premature death. Efforts to increase our understanding of AF and its complications have focused on unravelling the mechanisms of electrical and structural remodelling of the atrial myocardium. Yet, it is increasingly recognized that AF is more than an atrial disease, being associated with systemic inflammation, endothelial dysfunction, and adverse effects on the structure and function of the left ventricular myocardium tha...
Source: Cardiovascular Research - February 23, 2015 Category: Cardiology Authors: Wijesurendra, R. S., Casadei, B. Tags: REVIEW Source Type: research

miR-21: a star player in cardiac hypertrophy
(Source: Cardiovascular Research)
Source: Cardiovascular Research - February 23, 2015 Category: Cardiology Authors: Duygu, B., Da Costa Martins, P. A. Tags: EDITORIALS Source Type: research

Non-voltage-gated Ca2+ entry pathways in the heart: the untold STOrai?
(Source: Cardiovascular Research)
Source: Cardiovascular Research - February 23, 2015 Category: Cardiology Authors: Collins, H. E., Chatham, J. C. Tags: EDITORIALS Source Type: research

Contents Page
(Source: Cardiovascular Research)
Source: Cardiovascular Research - February 23, 2015 Category: Cardiology Tags: FRONT-MATTER/BACK-MATTER Source Type: research

Editorial Board
(Source: Cardiovascular Research)
Source: Cardiovascular Research - February 23, 2015 Category: Cardiology Tags: FRONT-MATTER/BACK-MATTER Source Type: research

Cover Page
(Source: Cardiovascular Research)
Source: Cardiovascular Research - February 23, 2015 Category: Cardiology Tags: FRONT-MATTER/BACK-MATTER Source Type: research

Aims and Scope
(Source: Cardiovascular Research)
Source: Cardiovascular Research - February 23, 2015 Category: Cardiology Tags: FRONT-MATTER/BACK-MATTER Source Type: research

Marine n-3 PUFAs modulate IKs gating, channel expression, and location in membrane microdomains
Conclusions We provide evidence that acute application of PUFAs increases Kv7.1/KCNE1 through a probably direct effect, and shows antiarrhythmic efficacy under IKr block. Conversely, chronic EPA application modifies the channel activity through a change in the Kv7.1/KCNE1 voltage-dependence, correlated with a redistribution of Kv7.1 over the cell membrane. This loss of function may be pro-arrhythmic. This shed light on the controversial effects of PUFAs regarding arrhythmias. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 16, 2015 Category: Cardiology Authors: Moreno, C., de la Cruz, A., Oliveras, A., Kharche, S. R., Guizy, M., Comes, N., Stary, T., Ronchi, C., Rocchetti, M., Baro, I., Loussouarn, G., Zaza, A., Severi, S., Felipe, A., Valenzuela, C. Tags: Ion channels and arrhythmias Source Type: research

Dissecting abdominal aortic aneurysm in Ang II-infused mice: suprarenal branch ruptures and apparent luminal dilatation
Conclusion Our results are the first to describe apparent luminal dilatation, suprarenal branch ruptures, and intramural haematoma formation in dissecting abdominal aortic aneurysms in mice. Moreover, we validate and demonstrate the vast potential of phase contrast X-ray tomographic microscopy in cardiovascular small animal applications. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 16, 2015 Category: Cardiology Authors: Trachet, B., Fraga-Silva, R. A., Piersigilli, A., Tedgui, A., Sordet-Dessimoz, J., Astolfo, A., Van der Donckt, C., Modregger, P., Stampanoni, M. F. M., Segers, P., Stergiopulos, N. Tags: Vascular biology Source Type: research

Independent roles of the priming and the triggering of the NLRP3 inflammasome in the heart
Aims The NLRP3 inflammasome is activated in the ischaemic heart promoting caspase-1 activation, inflammation, and cell death. Ischaemic injury establishes both a priming signal (transcription of inflammasome components) and a trigger (NLRP3 activation). Whether NLRP3 activation, without priming, induces cardiac dysfunction and/or failure is unknown. The aim of this study was to assess the independent and complementary roles of the priming and the triggering signals in the heart, in the absence of ischaemia or myocardial injury. Methods and results We used mice with mutant NLRP3 (constitutively active), NLRP3-A350V, under ...
Source: Cardiovascular Research - January 16, 2015 Category: Cardiology Authors: Toldo, S., Mezzaroma, E., McGeough, M. D., Pena, C. A., Marchetti, C., Sonnino, C., Van Tassell, B. W., Salloum, F. N., Voelkel, N. F., Hoffman, H. M., Abbate, A. Tags: Cardiac biology and remodelling Source Type: research

Uncoupling protein 3 mediates H2O2 preconditioning-afforded cardioprotection through the inhibition of MPTP opening
Conclusion UCP3 mediates the cardioprotection of H2O2PC against I/R injury by preserving the mitochondrial function through inhibiting mPTP opening via the interaction with ANT and the PI3K/Akt pathway. Our findings reveal novel mechanisms of UCP3 in the cardioprotection. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 16, 2015 Category: Cardiology Authors: Chen, Y., Liu, J., Zheng, Y., Wang, J., Wang, Z., Gu, S., Tan, J., Jing, Q., Yang, H. Tags: Cardiac biology and remodelling Source Type: research

Renalase is a novel target gene of hypoxia-inducible factor-1 in protection against cardiac ischaemia-reperfusion injury
Conclusion These findings have revealed renalase as a novel target gene of HIF-1α in protection against myocardial I/R injury, which provided a basis for therapeutic strategies for enhancing cardiomyocyte survival in patients associated with ischaemic heart diseases. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 16, 2015 Category: Cardiology Authors: Du, M., Huang, K., Huang, D., Yang, L., Gao, L., Wang, X., Huang, D., Li, X., Wang, C., Zhang, F., Wang, Y., Cheng, M., Tong, Q., Qin, G., Huang, K., Wang, L. Tags: Cardiac biology and remodelling Source Type: research

Na+ ions as spatial intracellular messengers for co-ordinating Ca2+ signals during pH heterogeneity in cardiomyocytes
Conclusions Na+ ions are rapidly diffusible messengers that expand the spatial scale of cytoplasmic pH–CaT interactions, helping to co-ordinate global Ca2+ signalling during conditions of intracellular pH non-uniformity. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 16, 2015 Category: Cardiology Authors: Swietach, P., Spitzer, K. W., Vaughan-Jones, R. D. Tags: Cardiac biology and remodelling Source Type: research

Physiological activation of Akt by PHLPP1 deletion protects against pathological hypertrophy
Conclusion Our data suggest that enhancing Akt activity by inhibiting its PHLPP1-mediated dephosphorylation promotes processes associated with physiological hypertrophy that may be beneficial in attenuating the development of pathological hypertrophy. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 16, 2015 Category: Cardiology Authors: Moc, C., Taylor, A. E., Chesini, G. P., Zambrano, C. M., Barlow, M. S., Zhang, X., Gustafsson, A. B., Purcell, N. H. Tags: Cardiac biology and remodelling Source Type: research

Deficiency of filamin A in endothelial cells impairs left ventricular remodelling after myocardial infarction
Conclusion Deletion of FLNA in ECs aggravated MI-induced LV dysfunction and cardiac failure as a result of defective endothelial response and increased scar formation by impaired endothelial function and signalling. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 16, 2015 Category: Cardiology Authors: Bandaru, S., Gronros, J., Redfors, B., Cil, C., Pazooki, D., Salimi, R., Larsson, E., Zhou, A.-X., Omerovic, E., Akyurek, L. M. Tags: Cardiac biology and remodelling Source Type: research

Optogenetic release of norepinephrine from cardiac sympathetic neurons alters mechanical and electrical function
Conclusion This study characterizes a powerful and clinically relevant new model for studies of cardiac arrhythmias generated by increasing the activity of sympathetic nerve terminals and the resulting activation of myocyte β-adrenergic receptors. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 16, 2015 Category: Cardiology Authors: Wengrowski, A. M., Wang, X., Tapa, S., Posnack, N. G., Mendelowitz, D., Kay, M. W. Tags: Integrative physiology and pathophysiology Source Type: research