Letter in response to remote ischaemic conditioning provides humoral cross-species cardioprotection through glycine receptor activation
We read with great interest the study by Alburquerque-B éjaret al.1 recently published inCardiovascular Research reporting that the cardioprotective effect of remote ischaemic conditioning (RIC) is related to remote glycine release in blood. Even if the protective mechanism of glycine remains unidentified, these results must be emphasized in the context of recent data reporting similar key involvement of glycine in human and rat with the use of different metabolomics techniques.2,3 Nevertheless, several other metabolites have been identified as potential effectors of RIC-induced protection such as kynurenine and kyn...
Source: Cardiovascular Research - February 21, 2017 Category: Cardiology Source Type: research

MiR-33 regulation of stretch-induced intimal hyperplasia in vein grafts
This editorial refers to ‘MicroRNA-33 protects against neointimal hyperplasia induced by arterial mechanical stretch in the grafted vein’ by K. Huang et al., pp. 488–497. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 21, 2017 Category: Cardiology Source Type: research

Topiramate modulates post-infarction inflammation primarily by targeting monocytes or macrophages
ConclusionControl of the GABAA receptor activity in monocytes/macrophages can potently modulate post-infarction inflammation. Topiramate emerges as a promising drug, which may be feasible to translate for MI therapy in the future. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 17, 2017 Category: Cardiology Source Type: research

Transforming growth factor β receptor inhibition prevents ventricular fibrosis in a mouse model of progressive cardiac conduction disease
ConclusionMyocardial fibrosis secondary to a loss of NaV1.5 is triggered by TGF-β signalling pathway. Those events are more likely secondary to the decreased NaV1.5 sarcolemmal expression rather than the decreased Na+ current per se. TGF-β receptor inhibition prevents age-dependent development of ventricular fibrosis in Scn5a+/− mouse. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 17, 2017 Category: Cardiology Source Type: research

Metabolic cardiomyopathies: fighting the next epidemic
(Source: Cardiovascular Research)
Source: Cardiovascular Research - February 16, 2017 Category: Cardiology Source Type: research

Ablation of periostin inhibits post-infarction myocardial regeneration in neonatal mice mediated by the phosphatidylinositol 3 kinase/glycogen synthase kinase 3 β/cyclin D1 signalling pathway
ConclusionAblation of periostin suppresses post-infarction myocardial regeneration by inhibiting the PI3K/GSK3 β/cyclin D1 signalling pathway, indicating that periostin is essential for myocardial regeneration. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 14, 2017 Category: Cardiology Source Type: research

Endothelial LOX-1 activation differentially regulates arterial thrombus formation depending on oxLDL levels: role of the Oct-1/SIRT1 and ERK1/2 pathways
ConclusionsThus, LOX-1 differentially regulates thrombus formation in vivo depending on the degree of activation by oxLDL. At low oxLDL levels LOX-1 activates the protective Oct-1/SIRT1 pathway, while at higher levels of the lipoprotein switches to the thrombogenic ERK1/2 pathway. These findings may be important for arterial thrombus formation in ACS and suggest that SIRT1 may represent a novel therapeutic target in this context. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 11, 2017 Category: Cardiology Source Type: research

Metabolic remodelling in diabetic cardiomyopathy
AbstractDiabetes is a risk factor for heart failure and cardiovascular mortality with specific changes to myocardial metabolism, energetics, structure, and function. The gradual impairment of insulin production and signalling in diabetes is associated with elevated plasma fatty acids and increased myocardial free fatty acid uptake and activation of the transcription factor PPARα. The increased free fatty acid uptake results in accumulation of toxic metabolites, such as ceramide and diacylglycerol, activation of protein kinase C, and elevation of uncoupling protein-3. Insulin signalling and glucose uptake/oxidation be...
Source: Cardiovascular Research - February 8, 2017 Category: Cardiology Source Type: research

Endothelial glycocalyx breakdown is mediated by angiopoietin-2
ConclusionOur data indicate that eGC breakdown is mediated by Angpt-2 in a non-redundant manner. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 6, 2017 Category: Cardiology Source Type: research

Elucidating arrhythmogenic mechanisms of long-QT syndrome CALM1 -F142L mutation in patient-specific induced pluripotent stem cell-derived cardiomyocytes
ConclusionThe main functional derangement in CALM1-F142L was prolonged repolarization with altered rate-dependency and sensitivity to β-adrenergic stimulation. Impaired CDI of ICaL underlined the electrical abnormality, which was sensitive to ICaL blockade. High mutation penetrance was confirmed in the presence of the native genotype, implying strong dominance of effects. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 2, 2017 Category: Cardiology Source Type: research

Barth syndrome cardiomyopathy
AbstractBarth syndrome (BTHS) is an inherited form of cardiomyopathy, caused by a mutation within the gene encoding the mitochondrial transacylase tafazzin. Tafazzin is involved in the biosynthesis of the unique phospholipid cardiolipin (CL), which is almost exclusively found in mitochondrial membranes. CL directly interacts with a number of essential protein complexes in the mitochondrial membranes including the respiratory chain, mitochondrial metabolite carriers, and proteins, involved in shaping mitochondrial morphology. Here we describe, how in BTHS CL deficiency causes changes in the morphology of mitochondria, struc...
Source: Cardiovascular Research - February 2, 2017 Category: Cardiology Source Type: research

JAK-STAT signalling and the atrial fibrillation promoting fibrotic substrate
ConclusionsHF activates the LA JAK-STAT system and enhances PDGF-signalling. JAK-STAT inhibition reduces the profibrotic effects of PDGF stimulation on canine fibroblasts in vitro while attenuating in vivo LA-fibrosis and remodelling in post-MI mice, suggesting that the JAK/STAT pathway contributes to LA-fibrogenesis and might be a potential target for LA-fibrosis prevention. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 2, 2017 Category: Cardiology Source Type: research

Osteopontin RNA aptamer can prevent and reverse pressure overload-induced heart failure
ConclusionTaken together, these data demonstrate that tuning down cardiac OPN signalling by an OPN RNA aptamer is a novel and effective approach for preventing cardiac hypertrophy and fibrosis, improving cardiac function, and reversing pressure overload-induced heart failure. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 1, 2017 Category: Cardiology Source Type: research

Sex differences in metabolic cardiomyopathy
AbstractIn contrast to ischemic cardiomyopathies which are more common in men, women are over-represented in diabetic cardiomyopathies. Diabetes is a risk factor for cardiovascular disease; however, there is a sexual dimorphism in this risk factor: heart disease is five times more common in diabetic women but only two-times more common in diabetic men. Heart failure with preserved ejection fraction, which is associated with metabolic syndrome, is also more prevalent in women. This review will examine potential mechanisms for the sex differences in metabolic cardiomyopathies. Sex differences in metabolism, calcium handling,...
Source: Cardiovascular Research - February 1, 2017 Category: Cardiology Source Type: research

The subcellular localization of neuronal nitric oxide synthase determines the downstream effects of NO on myocardial function
AimsIn healthy hearts, the neuronal nitric oxide synthase (nNOS) is predominantly localized to the sarcoplasmic reticulum (SR), where it regulates the ryanodine receptor Ca2+ release channel (RyR2) and phospholamban (PLB) phosphorylation, and to a lesser extent to the sarcolemmal membrane where it inhibits the L-type Ca2+ current (ICa). However, in failing hearts, impaired relaxation and depressed inotropy are associated with a larger proportion of nNOS being localized to the sarcolemmal membrane. Whether there is a causal relationship between altered myocardial function and subcellular localization of nNOS r...
Source: Cardiovascular Research - February 1, 2017 Category: Cardiology Source Type: research

Circular RNAs and heart failure: new players for an old disease
This editorial refers to ‘A landscape of circular RNA expression in the human heart’ by W.L.W. Tan et al., pp. 298–309. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 1, 2017 Category: Cardiology Source Type: research

Partitioning the heritability of coronary artery disease highlights the importance of immune-mediated processes and epigenetic sites associated with transcriptional activity
ConclusionsMore individual SNP associations will be detected for CAD as sample size increases. The identified modules provide further biological insight for CAD and highlight the importance of immune-mediated processes in CAD pathogenesis. Finally, we showed that genetic liability to CAD is mainly attributed to epigenetic sites associated with transcriptional activity which encourage the design of custom sequencing/genotyping panels based on transcriptionally active regions. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 31, 2017 Category: Cardiology Source Type: research

MicroRNA-33 protects against neointimal hyperplasia induced by arterial mechanical stretch in the grafted vein
ConclusionThe miR-33-BMP3-smad signalling pathway protects against venous SMC proliferation in response to the arterial stretch. miR-33 is a target that attenuates neointimal hyperplasia in grafted vessels and may have potential clinical applications. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 29, 2017 Category: Cardiology Source Type: research

Retraction of: abstract P71, In vitro and in vivo direct monitoring of miRNA-22 expression in isoproterenol-induced cardiac hypertrophy by bioluminescence imaging
(Source: Cardiovascular Research)
Source: Cardiovascular Research - January 23, 2017 Category: Cardiology Authors: Tu, Y., Wan, L., Bu, L., Shen, B. Tags: Corrigendum Source Type: research

Corrigendum to: HIF-2{alpha}-mediated induction of pulmonary thrombospondin-1 contributes to hypoxia-driven vascular remodelling and vasoconstriction
(Source: Cardiovascular Research)
Source: Cardiovascular Research - January 23, 2017 Category: Cardiology Tags: Corrigendum Source Type: research

Mitochondrial redox plays a critical role in the paradoxical effects of NAPDH oxidase-derived ROS on coronary endothelium
Conclusion The findings suggest that NOX-derived ROS results in increased mito-ROS. Whereas short-term increase in mito-ROS was counteracted by MnSOD, long-term increase in ROS resulted in nitrotyrosine-mediated inactivation of MnSOD, leading to unchecked increase in mito-ROS and loss of m followed by inhibition of endothelial function and proliferation. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 23, 2017 Category: Cardiology Authors: Shafique, E., Torina, A., Reichert, K., Colantuono, B., Nur, N., Zeeshan, K., Ravichandran, V., Liu, Y., Feng, J., Zeeshan, K., Benjamin, L. E., Irani, K., Harrington, E. O., Sellke, F. W., Abid, M. R. Tags: Vascular biology Source Type: research

The neuronal transcription factor NPAS4 is a strong inducer of sprouting angiogenesis and tip cell formation
Conclusions NPAS4 is expressed in endothelial cells, regulates VE-cadherin expression and regulates sprouting angiogenesis. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 23, 2017 Category: Cardiology Authors: Esser, J. S., Charlet, A., Schmidt, M., Heck, S., Allen, A., Lother, A., Epting, D., Patterson, C., Bode, C., Moser, M. Tags: Vascular biology Source Type: research

Tweak up-regulates endothelin-1 system in mouse and human endothelial cells
Conclusions In pathological situations such as chronic inflammation, TWEAK could be more harmful through this effect at endothelial level. Pharmacological blockade of this cytokine could prevent the haemodynamic and structural changes related to an increased ET-1 synthesis. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 23, 2017 Category: Cardiology Authors: Martinez-Miguel, P., Medrano-Andres, D., Griera-Merino, M., Ortiz, A., Rodriguez-Puyol, M., Rodriguez-Puyol, D., Lopez-Ongil, S. Tags: Vascular biology Source Type: research

At the cross-point of connexins, calcium, and ATP: blocking hemichannels inhibits vasoconstriction of rat small mesenteric arteries
Conclusions These results indicate that Cx43 hemichannels contribute to SMC Ca2+ dynamics and contractility, by facilitating Ca2+ entry, ATP release, and purinergic signalling. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 23, 2017 Category: Cardiology Authors: Bol, M., Wang, N., De Bock, M., Wacquier, B., Decrock, E., Gadicherla, A., Decaluwe, K., Vanheel, B., van Rijen, H. V. M., Krysko, D. V., Bultynck, G., Dupont, G., Van de Voorde, J., Leybaert, L. Tags: Vascular biology Source Type: research

Attenuation of carotid neointimal formation after direct delivery of a recombinant adenovirus expressing glucagon-like peptide-1 in diabetic rats
Aims Enhancement of glucagon-like peptide-1 (GLP-1) reduces glucose levels and preserves pancreatic β-cell function, but its effect against restenosis is unknown. Methods and results We investigated the effect of subcutaneous injection of exenatide or local delivery of a recombinant adenovirus expressing GLP-1 (rAd-GLP-1) into carotid artery, in reducing the occurrence of restenosis following balloon injury. As a control, we inserted β-galactosidase cDNA in the same vector (rAd-βGAL). Otsuka Long-Evans Tokushima rats were assigned to three groups (n = 12 each): (1) normal saline plus rAd-βGAL delivery ...
Source: Cardiovascular Research - January 23, 2017 Category: Cardiology Authors: Lim, S., Lee, G. Y., Park, H. S., Lee, D.-H., Tae Jung, O., Kyoung Min, K., Kim, Y.-B., Jun, H.-S., Hak Chul, J., Park, K. S. Tags: Vascular biology Source Type: research

Inhibition of SRF/myocardin reduces aortic stiffness by targeting vascular smooth muscle cell stiffening in hypertension
Aims Increased aortic stiffness is a fundamental manifestation of hypertension. However, the molecular mechanisms involved remain largely unknown. We tested the hypothesis that abnormal intrinsic vascular smooth muscle cell (VSMC) mechanical properties in large arteries, but not in distal arteries, contribute to the pathogenesis of aortic stiffening in hypertension, mediated by the serum response factor (SRF)/myocardin signalling pathway. Methods and results Four month old male spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats were studied. Using atomic force microscopy, significant VSMC stiff...
Source: Cardiovascular Research - January 23, 2017 Category: Cardiology Authors: Zhou, N., Lee, J.-J., Stoll, S., Ma, B., Wiener, R., Wang, C., Costa, K. D., Qiu, H. Tags: Vascular biology Source Type: research

A novel fission-independent role of dynamin-related protein 1 in cardiac mitochondrial respiration
Conclusion These results uncover a novel non-canonical function of the fission protein, DRP1 in maintaining or positively stimulating mitochondrial respiration, bioenergetics and ROS signalling in adult cardiomyocyte, which is likely independent of morphological changes. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 23, 2017 Category: Cardiology Authors: Zhang, H., Wang, P., Bisetto, S., Yoon, Y., Chen, Q., Sheu, S.-S., Wang, W. Tags: Cardiac biology and remodelling Source Type: research

Loss of AKAP150 promotes pathological remodelling and heart failure propensity by disrupting calcium cycling and contractile reserve
Conclusions These findings define a critical role for AKAP150 in regulating Ca2+ cycling and myocardial ionotropy following pathological stress, suggesting the AKAP150 signalling pathway may serve as a novel therapeutic target for heart failure. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 23, 2017 Category: Cardiology Authors: Li, L., Li, J., Drum, B. M., Chen, Y., Yin, H., Guo, X., Luckey, S. W., Gilbert, M. L., McKnight, G. S., Scott, J. D., Santana, L. F., Liu, Q. Tags: Cardiac biology and remodelling Source Type: research

ATF3 expression in cardiomyocytes preserves homeostasis in the heart and controls peripheral glucose tolerance
Conclusions Cardiac ATF3 has a protective role in dampening the HFD-induced cardiac remodeling processes. ATF3 exerts both local and systemic effects related to T2D-induced cardiomyopathy. This study provides a strong relationship between heart remodeling processes and blood glucose homeostasis. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 23, 2017 Category: Cardiology Authors: Kalfon, R., Koren, L., Aviram, S., Schwartz, O., Hai, T., Aronheim, A. Tags: Cardiac biology and remodelling Source Type: research

Sphingosine-1-phosphate signalling--a key player in the pathogenesis of Angiotensin II-induced hypertension
Conclusion The presented results point to a critical involvement of S1P and its signalling axis in the pathogenesis of hypertension. Specifically, SphK2 evolves as key player in immune cell trafficking and vascular dysfunction contributing to the development of overt hypertension. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 23, 2017 Category: Cardiology Authors: Meissner, A., Miro, F., Jimenez-Altayo, F., Jurado, A., Vila, E., Planas, A. M. Tags: Integrative physiology and pathophysiology Source Type: research

SRF/myocardin: a novel molecular axis regulating vascular smooth muscle cell stiffening in hypertension
(Source: Cardiovascular Research)
Source: Cardiovascular Research - January 23, 2017 Category: Cardiology Authors: Lacolley, P., Li, Z., Challande, P., Regnault, V. Tags: Invited Editorials Source Type: research

A new side to an old coin: dynamin related protein-1 with benefits in the heart
(Source: Cardiovascular Research)
Source: Cardiovascular Research - January 23, 2017 Category: Cardiology Authors: Konstantinidis, K. Tags: Invited Editorials Source Type: research

Akap-mediated signalling: the importance of being in the right place at the right time
(Source: Cardiovascular Research)
Source: Cardiovascular Research - January 23, 2017 Category: Cardiology Authors: Perrino, C., Trimarco, B. Tags: Invited Editorials Source Type: research

A novel protective role for activating transcription factor 3 in the cardiac response to metabolic stress
(Source: Cardiovascular Research)
Source: Cardiovascular Research - January 23, 2017 Category: Cardiology Authors: Ghigo, A., Frati, G., Sciarretta, S. Tags: Invited Editorials Source Type: research

Serelaxin treatment promotes adaptive hypertrophy but does not prevent heart failure in experimental peripartum cardiomyopathy
ConclusionAlthough Relaxin-2 levels seemed lower in PPCM patients diagnosed early postpartum, we observed a high pregnancy-related variance of serum Relaxin-2 levels peripartum making it unsuitable as a biomarker for this condition. Supplementation with sRlx may contribute to angiogenesis and compensatory hypertrophy in the diseased heart, but the effects are not sufficient to prevent heart failure in an experimental PPCM model. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 20, 2017 Category: Cardiology Source Type: research

SK channel enhancers attenuate Ca 2+ -dependent arrhythmia in hypertrophic hearts by regulating mito-ROS-dependent oxidation and activity of RyR
ConclusionThese data suggest that enhancement of mSK channels in hypertrophic rat hearts protects from Ca2+-dependent arrhythmia and suggest that the protection is mediated via decreased mitochondrial ROS and subsequent decreased oxidation of reactive cysteines in RyR, which ultimately leads to stabilization of RyR-mediated Ca2+ release. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 17, 2017 Category: Cardiology Source Type: research

Mitochondrial redox plays a critical role in the paradoxical effects of NAPDH oxidase-derived ROS on coronary endothelium
ConclusionThe findings suggest that NOX-derived ROS results in increased mito-ROS. Whereas short-term increase in mito-ROS was counteracted by MnSOD, long-term increase in ROS resulted in nitrotyrosine-mediated inactivation of MnSOD, leading to unchecked increase in mito-ROS and loss of Δψm followed by inhibition of endothelial function and proliferation. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 14, 2017 Category: Cardiology Source Type: research

The neuronal transcription factor NPAS4 is a strong inducer of sprouting angiogenesis and tip cell formation
ConclusionsNPAS4 is expressed in endothelial cells, regulates VE-cadherin expression and regulates sprouting angiogenesis. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 12, 2017 Category: Cardiology Source Type: research

Corrigendum to: HIF-2α-mediated induction of pulmonary thrombospondin-1 contributes to hypoxia-driven vascular remodelling and vasoconstriction
Corrigendum to: HIF-2α-mediated induction of pulmonary thrombospondin-1 contributes to hypoxia-driven vascular remodelling and vasoconstriction [Cardiovasc Res 2016; 109 (1): 115–130] (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 12, 2017 Category: Cardiology Source Type: research

Reperfusion therapy with recombinant human relaxin-2 (Serelaxin) attenuates myocardial infarct size and NLRP3 inflammasome following ischemia/reperfusion injury via eNOS-dependent mechanism
AimsThe preconditioning-like infarct-sparing and anti-inflammatory effects of the peptide hormone relaxin following ischemic injury have been studied in the heart. Whether reperfusion therapy with recombinant human relaxin-2, serelaxin, reduces myocardial infarct size and attenuates the subsequent NLRP3 inflammasome activation leading to further loss of functional myocardium following ischemia/reperfusion (I/R) injury is unknown.Methods and resultsAfter baseline echocardiography, adult male wild-type C57BL or eNOS knockout mice underwent myocardial infarction (MI) by coronary artery ligation for 30  min followed by ...
Source: Cardiovascular Research - January 10, 2017 Category: Cardiology Source Type: research

Exosomal miR-142-3p is increased during cardiac allograft rejection and augments vascular permeability through down-regulation of endothelial RAB11FIP2 expression
ConclusionWe have identified a novel mechanism whereby miR-142-3p, a microRNA enriched in exosomes during acute cellular rejection, is transferred to endothelial cells and compromises endothelial barrier function via down-regulation of RAB11FIP2. This study sheds new light on the interaction between host immune system and cardiac allograft endothelium during acute cellular rejection. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 10, 2017 Category: Cardiology Source Type: research

Optogenetic manipulation of anatomical re-entry by light-guided generation of a reversible local conduction block
ConclusionsAnatomical re-entry in ventricular tissue can be manipulated by optogenetic induction of a local and reversible conduction block in the re-entrant pathway, allowing effective re-entry termination. These results provide distinctively new mechanistic insight into re-entry termination and a novel perspective for cardiac arrhythmia management. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 10, 2017 Category: Cardiology Source Type: research

Sensitized signalling between L-type Ca 2+ channels and ryanodine receptors in the absence or inhibition of FKBP12.6 in cardiomyocytes
Conclusion:FKBP12.6 keeps the RyRs from over-sensitization, stabilizes the potentially regenerative CICR system, and thus may suppress the life-threatening arrhythmogenesis. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 10, 2017 Category: Cardiology Source Type: research

Corrigendum
to: Endothelial repair in stented arteries is accelerated by inhibition of Rho-associated protein kinase [Cardiovasc Res 2016;112:689–701] (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 9, 2017 Category: Cardiology Source Type: research

Refining the molecular organization of the cardiac intercalated disc
This review presents an extensively integrated model of the cardiac intercalated disc (ID), a highly orchestrated structure that connects adjacent cardiomyocytes. Classically, three main structures are distinguished: gap junctions (GJs) metabolically and electrically connect cytoplasm of adjacent cardiomyocytes; adherens junctions (AJs) connect the actin cytoskeleton of adjacent cells; and desmosomes function as cell anchors and connect intermediate filaments. Furthermore, ion channels reside in the ID. Mutations in ID proteins have been associated with cardiac arrhythmias such as Brugada syndrome and arrhythmogenic cardio...
Source: Cardiovascular Research - January 9, 2017 Category: Cardiology Source Type: research

Down-regulation of proangiogenic microRNA-126 and microRNA-132 are early modulators of diabetic cardiac microangiopathy
ConclusionsThese novel findings demonstrate that the down-regulation of angiomiRs is a major underlying mechanism for the development of microangiopathy in diabetic hearts. Therefore, therapeutic restoration of angiomiRs could become a potential approach to combat the cardiovascular complications of diabetes. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 9, 2017 Category: Cardiology Source Type: research

Angiopoietin-1 promotes atherosclerosis by increasing the proportion of circulating Gr1 + monocytes
ConclusionsAng-1 specifically increases circulating Gr1+ inflammatory monocytes and increases monocyte/macrophage retention in atherosclerotic plaques, thereby contributing to development of atherosclerosis. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 9, 2017 Category: Cardiology Source Type: research

Remote ischemic conditioning provides humoural cross-species cardioprotection through glycine receptor activation
AimsRemote ischaemic conditioning (RIC) releases a humoural factor able to exert cross-species cardioprotection when plasma dialysate is applied to isolated hearts. However, the exact chemical nature of this factor is currently unknown.Methods and resultsRIC (4 × 5min femoral occlusion/5min reperfusion) was applied to 10 male pigs, and blood was taken before and after the manoeuvre. Discriminant analysis of 1H-NMR spectra (n = 10–12) obtained from plasma dialysates (12–14 kDa cut-off) allowed to demonstrate a different metabolic profile between control and postRIC samples, with lactat...
Source: Cardiovascular Research - January 9, 2017 Category: Cardiology Source Type: research

Multilevel analyses of SCN5A mutations in arrhythmogenic right ventricular dysplasia/cardiomyopathy suggest non-canonical mechanisms for disease pathogenesis
AimsArrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy (ARVD/C) is often associated with desmosomal mutations. Recent studies suggest an interaction between the desmosome and sodium channel protein Nav1.5. We aimed to determine the prevalence and biophysical properties of mutations in SCN5A (the gene encoding Nav1.5) in ARVD/C.Methods and resultsWe performed whole-exome sequencing in six ARVD/C patients (33% male, 38.2 ± 12.1 years) without a desmosomal mutation. We found a rare missense variant (p.Arg1898His; R1898H) in SCN5A in one patient. We generated induced pluripotent stem cell-derived ca...
Source: Cardiovascular Research - January 9, 2017 Category: Cardiology Source Type: research

Reply: Glucagon-like peptide-1 mediates cardioprotection by remote ischaemic conditioning
We read with interest the Letter by Drs Giblett and Hoole in response to our research article ‘Glucagon-Like Peptide-1 (GLP-1) Mediates Cardioprotection by Remote Ischaemic Conditioning’.1 We thank Drs Giblett and Hoole for their interest in our work and provide our responses to the critical comments raised. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 9, 2017 Category: Cardiology Source Type: research