Genetic lineage tracing discloses arteriogenesis as the main mechanism for collateral growth in the mouse heart
Conclusion Apln-CreER-mediated lineage tracing distinguishes capillaries from large arteries, in both the neonatal and adult hearts. Through genetic fate mapping, we demonstrate that pre-existing arteries, but not capillaries, extensively contribute to collateral artery formation following myocardial injury. These results suggest that arteriogenesis is the major mechanism underlying collateral vessel formation. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 12, 2016 Category: Cardiology Authors: He, L., Liu, Q., Hu, T., Huang, X., Zhang, H., Tian, X., Yan, Y., Wang, L., Huang, Y., Miquerol, L., Wythe, J. D., Zhou, B. Tags: Vascular Biology Source Type: research

A novel role of endothelium in activation of latent pro-membrane type 1 MMP and pro-MMP-2 in rat aorta
Conclusions We propose that the endothelium under ANGII stimulation acts as a novel and key activator of latent pro-MT1MMP and pro-MMP2 in SMCs of rat aorta. Therefore, endothelium may critically contribute to pathophysiology of aortic stiffness. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 12, 2016 Category: Cardiology Authors: Otto, S., Deussen, A., Zatschler, B., Müller, B., Neisser, A., Barth, K., Morawietz, H., Kopaliani, I. Tags: Vascular Biology Source Type: research

Corrigendum to: Ilk conditional deletion in adult animals increases cyclic GMP-dependent vasorelaxation
(Source: Cardiovascular Research)
Source: Cardiovascular Research - February 12, 2016 Category: Cardiology Tags: CORRIGENDA Source Type: research

Cardiomyocyte exosomes regulate glycolytic flux in endothelium by direct transfer of GLUT transporters and glycolytic enzymes
Conclusion These findings establish CM-derived exosomes as key components of the cardio-endothelial communication system which, through intercellular protein complementation, would allow a rapid response from ECs to increase glucose transport and a putative uptake of metabolic fuels from blood to CMs. This CM–EC protein complementation process might have implications for metabolic regulation in health and disease. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 12, 2016 Category: Cardiology Authors: Garcia, N. A., Moncayo-Arlandi, J., Sepulveda, P., Diez-Juan, A. Tags: Cardiac biology and remodelling Source Type: research

Sphingosine-1-phosphate reduces ischaemia-reperfusion injury by phosphorylating the gap junction protein Connexin43
Conclusion Our study reveals an important molecular pathway by which modulating the apoM/S1P axis has a therapeutic potential in the fight against I/R injury in the heart. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 12, 2016 Category: Cardiology Authors: Morel, S., Christoffersen, C., Axelsen, L. N., Montecucco, F., Rochemont, V., Frias, M. A., Mach, F., James, R. W., Naus, C. C., Chanson, M., Lampe, P. D., Nielsen, M. S., Nielsen, L. B., Kwak, B. R. Tags: Cardiac biology and remodelling Source Type: research

Succinate dehydrogenase inhibition with malonate during reperfusion reduces infarct size by preventing mitochondrial permeability transition
Conclusion Succinate dehydrogenase inhibition with malonate at the onset of reperfusion reduces infarct size in isolated mice hearts through reduction in ROS production and mitochondrial permeability transition pore opening. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 12, 2016 Category: Cardiology Authors: Valls-Lacalle, L., Barba, I., Miro-Casas, E., Alburquerque-Bejar, J. J., Ruiz-Meana, M., Fuertes-Agudo, M., Rodriguez-Sinovas, A., Garcia-Dorado, D. Tags: Cardiac biology and remodelling Source Type: research

Corrigendum to: miR-30e targets IGF2-regulated osteogenesis in bone marrow-derived mesenchymal stem cells, aortic smooth muscle cells, and ApoE-/- mice
(Source: Cardiovascular Research)
Source: Cardiovascular Research - February 12, 2016 Category: Cardiology Tags: CORRIGENDA Source Type: research

Bidirectional cross-regulation between ErbB2 and {beta}-adrenergic signalling pathways
Conclusion Our studies show that myocardial ErbB2 and βAR signalling are linked in a feedback loop with βAR activation leading to increased ErbB2 expression and activity, and increased ErbB2 activity regulating β2AR expression. Most importantly, ErbB2 kinase activity is crucial for cardioprotection in the setting of β-adrenergic stress, suggesting that this mechanism is important in the pathophysiology and treatment of cardiomyopathy induced by ErbB2-targeting antineoplastic drugs. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 12, 2016 Category: Cardiology Authors: Sysa-Shah, P., Tocchetti, C. G., Gupta, M., Rainer, P. P., Shen, X., Kang, B.-H., Belmonte, F., Li, J., Xu, Y., Guo, X., Bedja, D., Gao, W. D., Paolocci, N., Rath, R., Sawyer, D. B., Naga Prasad, S. V., Gabrielson, K. Tags: Cardiac biology and remodelling Source Type: research

Neural crest-derived resident cardiac cells contribute to the restoration of adrenergic function of transplanted heart in rodent
Conclusion Neural crest-derived adrenergic cells increased following heart transplantation. The restoration of cardiac sympathetic activities in transplanted heart is tightly coupled with an increase in the number of neural crest-derived adrenergic cells. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 12, 2016 Category: Cardiology Authors: Tamura, Y., Sano, M., Nakamura, H., Ito, K., Sato, Y., Shinmura, K., Ieda, M., Fujita, J., Kurosawa, H., Ogawa, S., Nakano, S., Matsuzaki, M., Fukuda, K. Tags: Integrative physiology and pathophysiology Source Type: research

Adrenergic function restoration in the transplanted heart: a role for neural crest-derived cells
(Source: Cardiovascular Research)
Source: Cardiovascular Research - February 12, 2016 Category: Cardiology Authors: Mahmoud, A. I., Lee, R. T. Tags: EDITORIALS Source Type: research

PITX2: a master regulator of cardiac channelopathy in atrial fibrillation?
(Source: Cardiovascular Research)
Source: Cardiovascular Research - February 12, 2016 Category: Cardiology Authors: Li, N., Dobrev, D., Wehrens, X. H. T. Tags: EDITORIALS Source Type: research

Editorial Board
(Source: Cardiovascular Research)
Source: Cardiovascular Research - February 12, 2016 Category: Cardiology Tags: FRONT-MATTER/BACK-MATTER Source Type: research

Cover Page
(Source: Cardiovascular Research)
Source: Cardiovascular Research - February 12, 2016 Category: Cardiology Tags: FRONT-MATTER/BACK-MATTER Source Type: research

Contents Page
(Source: Cardiovascular Research)
Source: Cardiovascular Research - February 12, 2016 Category: Cardiology Tags: FRONT-MATTER/BACK-MATTER Source Type: research

Aims and Scope
(Source: Cardiovascular Research)
Source: Cardiovascular Research - February 12, 2016 Category: Cardiology Tags: FRONT-MATTER/BACK-MATTER Source Type: research

Toll-like receptor 3 signalling mediates angiogenic response upon shock wave treatment of ischaemic muscle
Conclusion Our data reveal a central role of the innate immune system, namely Toll-like receptor 3, to mediate angiogenesis upon release of cytoplasmic RNAs by mechanotransduction of SWT. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 25, 2016 Category: Cardiology Authors: Holfeld, J., Tepeköylü, C., Reissig, C., Lobenwein, D., Scheller, B., Kirchmair, E., Kozaryn, R., Albrecht-Schgoer, K., Krapf, C., Zins, K., Urbschat, A., Zacharowski, K., Grimm, M., Kirchmair, R., Paulus, P. Tags: Vascular Biology Source Type: research

Differential effects of tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2 on atherosclerosis and monocyte/macrophage invasion
Conclusion Our data demonstrate that TIMP-2 plays a greater protective role than TIMP-1 during the pathogenesis of atherosclerosis, in part by suppressing MMP-14-dependent monocyte/macrophage accumulation into plaques. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 25, 2016 Category: Cardiology Authors: Di Gregoli, K., George, S. J., Jackson, C. L., Newby, A. C., Johnson, J. L. Tags: Vascular Biology Source Type: research

A CD1d-dependent lipid antagonist to NKT cells ameliorates atherosclerosis in ApoE-/- mice by reducing lesion necrosis and inflammation
Conclusion The attenuation of progression of established atherosclerosis together with reduced development of atherosclerosis in hyperlipidaemic mice by the NKT antagonist, without affecting NKT cell or other lymphocyte numbers, suggests that targeting lesion inflammation via CD1d-dependent activation of NKT cells using DPPE-PEG350 has a therapeutic potential in treating atherosclerosis. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 25, 2016 Category: Cardiology Authors: Li, Y., Kanellakis, P., Hosseini, H., Cao, A., Deswaerte, V., Tipping, P., Toh, B.-H., Bobik, A., Kyaw, T. Tags: Vascular Biology Source Type: research

Enhanced atheroprotection and lesion remodelling by targeting the foam cell and increasing plasma cholesterol acceptors
Conclusion These studies demonstrate a mutually beneficial relationship between PLIN2 deficiency and elevated apoA-I/HDL-C in preventing atherosclerosis development. The data support that targeting foam cell components to mobilize cholesterol may be a promising strategy to enhance the atheroprotection of plasma cholesterol acceptors. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 25, 2016 Category: Cardiology Authors: Son, S.-H., Goo, Y.-H., Choi, M., Saha, P. K., Oka, K., Chan, L. C. B., Paul, A. Tags: Vascular Biology Source Type: research

Nanotherapeutics for inhibition of atherogenesis and modulation of inflammation in atherosclerotic plaques
Conclusions Sugar-based amphiphilic macromolecules can be complexed with α-T to establish new anti-athero-inflammatory nanotherapeutics. These dual efficacy NPs effectively inhibited key features of atherosclerosis (modified lipid uptake and the formation of foam cells) while demonstrating reduction in inflammatory markers based on a disease-mimetic model of human atherosclerotic plaques. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 25, 2016 Category: Cardiology Authors: Lewis, D. R., Petersen, L. K., York, A. W., Ahuja, S., Chae, H., Joseph, L. B., Rahimi, S., Uhrich, K. E., Haser, P. B., Moghe, P. V. Tags: Vascular Biology Source Type: research

Myeloid cell-derived LRG attenuates adverse cardiac remodelling after myocardial infarction
Conclusion LRG, produced by heart-infiltrating myeloid cells, suppresses adverse cardiac remodelling after MI as a novel cardioprotective factor. LRG signalling could be a therapeutic target against cardiovascular diseases. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 25, 2016 Category: Cardiology Authors: Kumagai, S., Nakayama, H., Fujimoto, M., Honda, H., Serada, S., Ishibashi-Ueda, H., Kasai, A., Obana, M., Sakata, Y., Sawa, Y., Fujio, Y., Naka, T. Tags: Cardiac biology and remodelling Source Type: research

Loss of plakoglobin immunoreactivity in intercalated discs in arrhythmogenic right ventricular cardiomyopathy: protein mislocalization versus epitope masking
Conclusions Reduced plakoglobin staining in intercalated discs of heart tissue from human ARVC patients and in a murine ARVC model is caused by alterations in epitope accessibility and not by protein relocalization. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 25, 2016 Category: Cardiology Authors: Kant, S., Krusche, C. A., Gaertner, A., Milting, H., Leube, R. E. Tags: Cardiac biology and remodelling Source Type: research

Deficiency of IL-12p35 improves cardiac repair after myocardial infarction by promoting angiogenesis
Conclusions Deficiency of IL-12p35 limited AMI-induced cardiac injury by promoting pro-angiogenesis and anti-inflammatory functions of monocytes. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 25, 2016 Category: Cardiology Authors: Kan, X., Wu, Y., Ma, Y., Zhang, C., Li, P., Wu, L., Zhang, S., Li, Y., Du, J. Tags: Cardiac biology and remodelling Source Type: research

Translational failure of anti-inflammatory compounds for myocardial infarction: a meta-analysis of large animal models
Aims Numerous anti-inflammatory drugs have been tested in large animal studies of myocardial infarction (MI). Despite positive results, translation of anti-inflammatory strategies into clinical practice has proved to be difficult. Critical disparities between preclinical and clinical study design that influence efficacy may partly be responsible for this translational failure. The aim of the present systematic review was to better understand which factors underlie the failure of transition towards the clinic. Methods and results Meta-analysis and regression of large animal studies were performed to identify sources that i...
Source: Cardiovascular Research - January 25, 2016 Category: Cardiology Authors: van Hout, G. P. J., Jansen of Lorkeers, S. J., Wever, K. E., Sena, E. S., Kouwenberg, L. H. J. A., van Solinge, W. W., Macleod, M. R., Doevendans, P. A., Pasterkamp, G., Chamuleau, S. A. J., Hoefer, I. E. Tags: Cardiac biology and remodelling Source Type: research

Integrative miRNA and whole-genome analyses of epicardial adipose tissue in patients with coronary atherosclerosis
Conclusion EAT in CAD is characterized by changes in the regulation of metabolism and inflammation with miR-103-3p/CCL13 pair as novel putative actors in EAT function and CAD. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 25, 2016 Category: Cardiology Authors: Vacca, M., Di Eusanio, M., Cariello, M., Graziano, G., D'Amore, S., Petridis, F. D., D'orazio, A., Salvatore, L., Tamburro, A., Folesani, G., Rutigliano, D., Pellegrini, F., Sabba, C., Palasciano, G., Di Bartolomeo, R., Moschetta, A. Tags: Integrative physiology and pathophysiology Source Type: research

Impaired Hedgehog signalling-induced endothelial dysfunction is sufficient to induce neuropathy: implication in diabetes
Conclusion The present work demonstrates the critical role of Dhh in maintaining blood nerve barrier integrity and demonstrates for the first time that endothelial dysfunction is sufficient to induce neuropathy. (Source: Cardiovascular Research)
Source: Cardiovascular Research - January 25, 2016 Category: Cardiology Authors: Chapouly, C., Yao, Q., Vandierdonck, S., Larrieu-Lahargue, F., Mariani, J. N., Gadeau, A.-P., Renault, M.-A. Tags: Integrative physiology and pathophysiology Source Type: research

Congenital coronary artery anomalies: a bridge from embryology to anatomy and pathophysiology--a position statement of the development, anatomy, and pathology ESC Working Group
Congenital coronary artery anomalies are of major significance in clinical cardiology and cardiac surgery due to their association with myocardial ischaemia and sudden death. Such anomalies are detectable by imaging modalities and, according to various definitions, their prevalence ranges from 0.21 to 5.79%. This consensus document from the Development, Anatomy and Pathology Working Group of the European Society of Cardiology aims to provide: (i) a definition of normality that refers to essential anatomical and embryological features of coronary vessels, based on the integrated analysis of studies of normal and abnormal co...
Source: Cardiovascular Research - January 25, 2016 Category: Cardiology Authors: Perez-Pomares, J. M., de la Pompa, J. L., Franco, D., Henderson, D., Ho, S. Y., Houyel, L., Kelly, R. G., Sedmera, D., Sheppard, M., Sperling, S., Thiene, G., van den Hoff, M., Basso, C. Tags: REVIEWS Source Type: research

Arteriovenous malformations in hereditary haemorrhagic telangiectasia: looking beyond ALK1-NOTCH interactions
Hereditary haemorrhagic telangiectasia (HHT) is characterized by the development of arteriovenous malformations—enlarged shunts allowing arterial flow to bypass capillaries and enter directly into veins. HHT is caused by mutations in ALK1 or Endoglin; however, the majority of arteriovenous malformations are idiopathic and arise spontaneously. Idiopathic arteriovenous malformations differ from those due to loss of ALK1 in terms of both location and disease progression. Furthermore, while arteriovenous malformations in HHT and Alk1 knockout models have decreased NOTCH signalling, some idiopathic arteriovenous malformat...
Source: Cardiovascular Research - January 25, 2016 Category: Cardiology Authors: Peacock, H. M., Caolo, V., Jones, E. A. V. Tags: REVIEWS Source Type: research

Perilipin2/adipophilin and ApoA-1 team up to combat atherosclerosis
(Source: Cardiovascular Research)
Source: Cardiovascular Research - January 25, 2016 Category: Cardiology Authors: Pourcet, B., Staels, B. Tags: EDITORIALS Source Type: research

Combination nanotherapy penetrates atherosclerosis
(Source: Cardiovascular Research)
Source: Cardiovascular Research - January 25, 2016 Category: Cardiology Authors: Mulder, W. J. M. Tags: EDITORIALS Source Type: research

Why does pre-clinical success in cardioprotection fail at the bedside?
(Source: Cardiovascular Research)
Source: Cardiovascular Research - January 25, 2016 Category: Cardiology Authors: Tritto, I., Ambrosio, G. Tags: EDITORIALS Source Type: research

Contents Page
(Source: Cardiovascular Research)
Source: Cardiovascular Research - January 25, 2016 Category: Cardiology Tags: FRONT-MATTER/BACK-MATTER Source Type: research

Editorial Board
(Source: Cardiovascular Research)
Source: Cardiovascular Research - January 25, 2016 Category: Cardiology Tags: FRONT-MATTER/BACK-MATTER Source Type: research

Cover Page
(Source: Cardiovascular Research)
Source: Cardiovascular Research - January 25, 2016 Category: Cardiology Tags: FRONT-MATTER/BACK-MATTER Source Type: research

Aims and Scope
(Source: Cardiovascular Research)
Source: Cardiovascular Research - January 25, 2016 Category: Cardiology Tags: FRONT-MATTER/BACK-MATTER Source Type: research

'(De-)sensitization vs. 'Uncoupling: what drives cardiomyopathies in the thin filament? Reply
(Source: Cardiovascular Research)
Source: Cardiovascular Research - December 28, 2015 Category: Cardiology Authors: Marston, S., Messer, A., Papadaki, M. Tags: LETTERS TO THE EDITOR Source Type: research

'(De-)sensitization vs. 'Uncoupling: what drives cardiomyopathies in the thin filament?
(Source: Cardiovascular Research)
Source: Cardiovascular Research - December 28, 2015 Category: Cardiology Authors: Hwang, P. M. Tags: LETTERS TO THE EDITOR Source Type: research

Nitrated fatty acids suppress angiotensin II-mediated fibrotic remodelling and atrial fibrillation
Conclusion OA-NO2 potently inhibits atrial fibrosis and subsequent AF. Nitro-fatty acids and possibly other lipid electrophiles thus emerge as potential therapeutic agents for AF, either by increasing endogenous levels through dietary modulation or by administration as synthetic drugs. (Source: Cardiovascular Research)
Source: Cardiovascular Research - December 28, 2015 Category: Cardiology Authors: Rudolph, T. K., Ravekes, T., Klinke, A., Friedrichs, K., Mollenhauer, M., Pekarova, M., Ambrozova, G., Martiskova, H., Kaur, J.-J., Matthes, B., Schwoerer, A., Woodcock, S. R., Kubala, L., Freeman, B. A., Baldus, S., Rudolph, V. Tags: Ion Channels and Arrhythmias Source Type: research

The renin-angiotensin system promotes arrhythmogenic substrates and lethal arrhythmias in mice with non-ischaemic cardiomyopathy
Conclusion Renin inhibition or genetic deletion of AT1aR suppresses pathological cardiac remodelling that leads to the generation of substrates maintaining VT/VF and reduces the occurrence of sudden death in dnNRSF-Tg mice. These findings demonstrate the significant contribution of RAS activation to the progression of arrhythmogenic substrates. (Source: Cardiovascular Research)
Source: Cardiovascular Research - December 28, 2015 Category: Cardiology Authors: Yamada, C., Kuwahara, K., Yamazaki, M., Nakagawa, Y., Nishikimi, T., Kinoshita, H., Kuwabara, Y., Minami, T., Yamada, Y., Shibata, J., Nakao, K., Cho, K., Arai, Y., Honjo, H., Kamiya, K., Nakao, K., Kimura, T. Tags: Ion Channels and Arrhythmias Source Type: research

Statins up-regulate SmgGDS through {beta}1-integrin/Akt1 pathway in endothelial cells
Conclusion These results indicate that statins selectively up-regulate SmgGDS in endothelial cells, for which the β1-integrin/Akt1 pathway may be involved, demonstrating the novel aspects of the pleiotropic effects of statins. (Source: Cardiovascular Research)
Source: Cardiovascular Research - December 28, 2015 Category: Cardiology Authors: Minami, T., Satoh, K., Nogi, M., Kudo, S., Miyata, S., Tanaka, S.-i., Shimokawa, H. Tags: Vascular Biology Source Type: research

Pim1 kinase promotes angiogenesis through phosphorylation of endothelial nitric oxide synthase at Ser-633
Conclusion Our findings demonstrate Pim1 as a novel kinase that is responsible for the phosphorylation of eNOS at Ser-633 and enhances EC sprouting of aortic rings from diabetic mice, suggesting that Pim1 could potentially serve as a novel therapeutic target for revascularization strategies. (Source: Cardiovascular Research)
Source: Cardiovascular Research - December 28, 2015 Category: Cardiology Authors: Chen, M., Yi, B., Zhu, N., Wei, X., Zhang, G.-X., Huang, S., Sun, J. Tags: Vascular Biology Source Type: research

Age-dependent blood pressure elevation is due to increased vascular smooth muscle tone mediated by G-protein signalling
Conclusion Age-dependent blood pressure elevation is due to a highly reversible activation of procontractile signalling in vascular smooth muscle cells indicating that increased vascular tone can be a primary factor in the development of hypertension. (Source: Cardiovascular Research)
Source: Cardiovascular Research - December 28, 2015 Category: Cardiology Authors: Wirth, A., Wang, S., Takefuji, M., Tang, C., Althoff, T. F., Schweda, F., Wettschureck, N., Offermanns, S. Tags: Vascular Biology Source Type: research

HIF-2{alpha}-mediated induction of pulmonary thrombospondin-1 contributes to hypoxia-driven vascular remodelling and vasoconstriction
Conclusions These findings demonstrate that HIF-2α is clearly implicated in the TSP1 pulmonary regulation and provide new insights on its contribution to PAH-driven vascular remodelling and vasoconstriction. (Source: Cardiovascular Research)
Source: Cardiovascular Research - December 28, 2015 Category: Cardiology Authors: Labrousse-Arias, D., Castillo-Gonzalez, R., Rogers, N. M., Torres-Capelli, M., Barreira, B., Aragones, J., Cogolludo, A., Isenberg, J. S., Calzada, M. J. Tags: Vascular Biology Source Type: research

Cardiac mTOR complex 2 preserves ventricular function in pressure-overload hypertrophy
Conclusion Our study demonstrates that mTORC2 is implicated in maintaining contractile function of the pressure-overloaded male mouse heart. (Source: Cardiovascular Research)
Source: Cardiovascular Research - December 28, 2015 Category: Cardiology Authors: Shende, P., Xu, L., Morandi, C., Pentassuglia, L., Heim, P., Lebboukh, S., Berthonneche, C., Pedrazzini, T., Kaufmann, B. A., Hall, M. N., Rüegg, M. A., Brink, M. Tags: Cardiac biology and remodelling Source Type: research

Ranolazine antagonizes catecholamine-induced dysfunction in isolated cardiomyocytes, but lacks long-term therapeutic effects in vivo in a mouse model of hypertrophic cardiomyopathy
Conclusion Ranolazine improved tolerance to high workload in mouse HCM cardiomyocytes, not by blocking late Na+ current, but by antagonizing β-adrenergic stimulation and slightly desensitizing myofilaments to Ca2+. This effect did not translate in therapeutic efficacy in vivo. (Source: Cardiovascular Research)
Source: Cardiovascular Research - December 28, 2015 Category: Cardiology Authors: Flenner, F., Friedrich, F. W., Ungeheuer, N., Christ, T., Geertz, B., Reischmann, S., Wagner, S., Stathopoulou, K., Söhren, K.-D., Weinberger, F., Schwedhelm, E., Cuello, F., Maier, L. S., Eschenhagen, T., Carrier, L. Tags: Cardiac biology and remodelling Source Type: research

Impaired mitochondrial network excitability in failing guinea-pig cardiomyocytes
Conclusion The disrupted inter-mitochondrial tethering and loss of structural organization may underlie decreased ROS-dependent mitochondrial coupling in HF. (Source: Cardiovascular Research)
Source: Cardiovascular Research - December 28, 2015 Category: Cardiology Authors: Goh, K. Y., Qu, J., Hong, H., Liu, T., Dell'Italia, L. J., Wu, Y., O'Rourke, B., Zhou, L. Tags: Cardiac biology and remodelling Source Type: research

Matrix cross-linking lysyl oxidases are induced in response to myocardial infarction and promote cardiac dysfunction
Conclusion LOX family members contribute significantly to the detrimental effects of cardiac remodelling, highlighting LOX inhibition as a potential therapeutic strategy for post-infarction recovery. (Source: Cardiovascular Research)
Source: Cardiovascular Research - December 28, 2015 Category: Cardiology Authors: Gonzalez-Santamaria, J., Villalba, M., Busnadiego, O., Lopez-Olaneta, M. M., Sandoval, P., Snabel, J., Lopez-Cabrera, M., Erler, J. T., Hanemaaijer, R., Lara-Pezzi, E., Rodriguez-Pascual, F. Tags: Cardiac biology and remodelling Source Type: research

Pitx2 impairs calcium handling in a dose-dependent manner by modulating Wnt signalling
Conclusion Our data demonstrate a dose-dependent relation between Pitx2 expression and the expression of AF susceptibility genes, calcium handling, and microRNAs and identify a complex regulatory network orchestrated by Pitx2 with large impact on atrial arrhythmogenesis susceptibility. (Source: Cardiovascular Research)
Source: Cardiovascular Research - December 28, 2015 Category: Cardiology Authors: Lozano-Velasco, E., Hernandez-Torres, F., Daimi, H., Serra, S. A., Herraiz, A., Hove-Madsen, L., Aranega, A., Franco, D. Tags: Cardiac biology and remodelling Source Type: research

Neuregulin-1 improves right ventricular function and attenuates experimental pulmonary arterial hypertension
Conclusion rhNRG-1 treatment attenuates pulmonary arterial and RV remodelling, and dysfunction in a rat model of MCT-induced PAH and has direct anti-remodelling effects on the pressure-overloaded RV. (Source: Cardiovascular Research)
Source: Cardiovascular Research - December 28, 2015 Category: Cardiology Authors: Mendes-Ferreira, P., Maia-Rocha, C., Adao, R., Mendes, M. J., Santos-Ribeiro, D., Alves, B. S., Cerqueira, R. J., Castro-Chaves, P., Lourenco, A. P., De Keulenaer, G. W., Leite-Moreira, A. F., Bras-Silva, C. Tags: Integrative physiology and pathophysiology Source Type: research

TRPC3 channel confers cerebrovascular remodelling during hypertension via transactivation of EGF receptor signalling
Conclusion Collectively, we demonstrated that enhanced EGFR transactivation, due to increased TRPC3 expression and functional coupling of TRPC3/ADAM17, resulted in cerebrovascular remodelling. Therefore, TRPC3-induced EGFR transactivation may be therapeutically exploited to prevent hypertension-induced cerebrovascular remodelling. (Source: Cardiovascular Research)
Source: Cardiovascular Research - December 28, 2015 Category: Cardiology Authors: Wang, M., Tang, Y.-B., Ma, M.-M., Chen, J.-H., Hu, C.-P., Zhao, S.-P., Peng, D.-Q., Zhou, J.-G., Guan, Y.-Y., Zhang, Z. Tags: Integrative physiology and pathophysiology Source Type: research