You have full text access to this Open Access content

EMBO Molecular Medicine

All articles accepted from 14 August 2012 are published under the terms of the Creative Commons Attribution License.   Articles accepted before this date were published under the agreement as stated in the final article.

Cover image for Vol. 9 Issue 9

Edited By: Philippe Sansonetti (Editor in Chief), Roberto Buccione and Céline Carret (EMBO Editors)

Online ISSN: 1757-4684

Review Series: Cardiovascular Diseases

Cardiovascular diseases are still the leading cause of death worldwide. Impaired endothelial function followed by inflammation of the vessel wall leads to atherosclerotic lesion formation that causes myocardial infarction and stroke. The increase of major risk factors such as obesity and diabetes in industrialized but also developing countries further increases the burden of vascular disease. In this Review Series, the authors cover important emerging fields in cardiovascular research and translation.


Christian Besler, Thomas F. Lüscher, Ulf Landmesser
EMBO Mol Med 2012, 4(4), 251–268
Low high-density lipoprotein-cholesterol levels are associated with an increased risk of coronary artery disease and myocardial infarction, which has triggered the hypothesis that HDL acts as an anti-atherogenic lipoprotein. In this Review, the role of high-density lipoprotein as an anti-atherogenic lipoprotein is discussed in detail.
Thomas Thum
EMBO Mol Med 2012, 4(1), 3-14
MicroRNAs are important and powerful mediators in a wide range of diseases including cardiovacsular diseases and thus emerged as interesting new drug targets. Here, the author discusses the current knowledge about miRNA therapeutics in cardiovascular diseases on their way to clinical use.
Rory R. Koenen, Christian Weber
EMBO Mol Med 2011, 3(12), 713-725
The chemokine system has been explored in search for therapeutic targets to prevent or treat inflammatory disorders, such as atherosclerosis. In this Review, the current standing of the dynamic field of chemokine-targeting therapeutics is highlighted and the potential advantages and drawbacks of particular strategies are discussed.
Matthew L. Steinhauser, Richard T. Lee
EMBO Mol Med 2011, 3(12), 701-712
The death of cardiac myocytes diminishes the heart's pump function and is a major cause of heart failure, one of the dominant causes of death worldwide. Here, the authors discuss cardiac regeneration as a potential therapeutic avenue with a focus on the challenges that hold back therapeutic development.

Further reading on Cardiovascular Diseases

Exon skipping is a promising therapy for selected genetic diseases. Here, the authors show as a proof-of-principle that MYBPC3 mutation-induced cardiomyopathy can be rescued by AAV-U7-antisense oligoribonucleotides in the heart of neonatal mice.
Christina Gedicke-Hornung, Verena Behrens-Gawlik, Silke Reischmann, Birgit Geertz, Doreen Stimpel, Florian Weinberger, Saskia Schlossarek, Guillaume Précigout, Ingke Braren, Thomas Eschenhagen, Giulia Mearini, Stéphanie Lorain, Thomas Voit, Patrick A. Dreyfus, Luis Garcia and Lucie Carrier
EMBO Mol Med 2013, 5(7), 1128–1145

TIE2-expressing macrophages switch towards an M2 phenotype following ischemia. ANG1/TIE2-signaling results in down-regulation of PHD2 and promotes arteriogenesis, suggesting new effective cell-based therapeutic approaches to treat limb ischemia.
Alexander Hamm, Lorenzo Veschini, Yukiji Takeda, Sandra Costa, Estelle Delamarre, Mario Leonardo Squadrito, Anne-Theres Henze, Mathias Wenes, Jens Serneels, Ferdinando Pucci, Carmen Roncal, Andrey Anisimov, Kari Alitalo, Michele De Palma, Massimiliano Mazzone
EMBO Mol Med 2013, 5(6), 843–857

Tie2-expressing macrophages (TEMs) have the potential to improve revascularization of the ischemic limb and may therefore, represent an attractive novel cell therapy for promoting limb salvage in patients suffering from critical limb ischemia.
Ashish S. Patel, Alberto Smith, Silvia Nucera, Daniela Biziato, Prakash Saha, Rizwan Q. Attia, Julia Humphries, Katherine Mattock, Steven P. Grover, Oliver T. Lyons, Luca G. Guidotti, Richard Siow, Aleksandar Ivetic, Stuart Egginton, Matthew Waltham, Luigi Naldini, Michele De Palma, Bijan Modarai
EMBO Mol Med 2013, 5(6), 858–869
Costanza Emanueli, Nicolle Kränkel
EMBO Mol Med 2013, 5(6), 802–804

Dilated cardiomyopathy is one the most frequent heart muscle diseases, which is responsible for one third of all heart failure cases. Here, the authors show widespread changes in DNA methylation patterns responsible for the disease.
Jan Haas, Karen S. Frese, Yoon Jung Park, Andreas Keller, Britta Vogel, Anders M. Lindroth, Dieter Weichenhan, Jennifer Franke, Simon Fischer, Andrea Bauer, Sabine Marquart, Farbod Sedaghat-Hamedani, Elham Kayvanpour, Doreen Köhler, Nadine M. Wolf, Sarah Hassel, Rouven Nietsch, Thomas Wieland, Philipp Ehlermann, Jobst-Hendrik Schultz, Andreas Dösch, Derliz Mereles, Stefan Hardt, Johannes Backs, Jörg D. Hoheisel, Christoph Plass, Hugo A. Katus, Benjamin Meder
EMBO Mol Med 2013, 5(3), 413–429

Cell therapy with cardiosphere-derived cells regenerates the infarcted adult mouse heart by increasing adult cardiomyocyte proliferation and recruiting endogenous stem cells.
Konstantinos Malliaras, Yiqiang Zhang, Jeffrey Seinfeld, Giselle Galang, Eleni Tseliou, Ke Cheng, Baiming Sun, Mohammad Aminzadeh, Eduardo Marbán
EMBO Mol Med 2013, 5(2), 191–209
Jose A. Palacios, Michael D. Schneider
EMBO Mol Med 2013, 5(2), 177–179

Persistent cardiac hypertrophy ultimately leads to cardiovascular disease. Here, the authors show that the nuclear receptor TR3 participates in angiotensin-induced cardiac hypertrophy by controlling mTORC1 signaling.
Rong-Hao Wang, Jian-Ping He, Mao-Long Su, Jie Luo, Ming Xu, Xiao-Dan Du, Hang-Zi Chen, Wei-Jia Wang, Yuan Wang, Nan Zhang, Bi-Xing Zhao, Wen-Xiu Zhao, Zhong-Gui Shan, Jiahuai Han, Chawnshang Chang, Qiao Wu
EMBO Mol Med 2013, 5(1), 137–148

Currently, the diagnosis of acute coronary syndrome (ACS) is based on elevation of (high-sensitive) cardiac troponins, which are not consistently elevated within the first hours after symptom onset. This study shows that circulating miRNAs hold great potential as novel early biomarkers of cardiac injury.
Martinus I. F. J. Oerlemans, Arend Mosterd, Marieke S. Dekker, Evelyn A. de Vrey, Alain van Mil, Gerard Pasterkamp, Pieter A. Doevendans, Arno W. Hoes, Joost P. G. Sluijter
EMBO Mol Med 2012, 4(11), 1176–1185

IL-13 has the capacity to alter plaque morphology in the presence of high serum cholesterol levels towards more stable, less vulnerable plaques. Because IL-13 leads to alternative macrophage activation in atherosclerotic lesions, and these macrophages have anti-atherogenic properties, the data identify macrophage polarization by IL-13 as novel point for therapeutic intervention.
Larissa Cardilo-Reis, Sabrina Gruber, Sabine M. Schreier, Maik Drechsler, Nikolina Papac-Milicevic, Christian Weber, Oswald Wagner, Herbert Stangl, Oliver Soehnlein, Christoph J. Binder
EMBO Mol Med 2012, 4(10), 1072–1086

The Wnt/beta-catenin pathway is essential for embryonic cardiogenesis, cardiac homeostasis and remodeling. Here, the authors show a novel interaction between KLF15 and beta-catenin/TCF4, which regulates cardiac progenitor cell fate in vivo.
Claudia Noack, Maria-Patapia Zafiriou, Hans-Joerg Schaeffer, Anke Renger, Elena Pavlova, Rainer Dietz, Wolfram H. Zimmermann, Martin W. Bergmann and Laura C. Zelarayán
EMBO Mol Med 2012, 4(9), 992–1007

Cardiac hypertrophy is associated with a substrate switch from fatty acid to glucose. Here, the authors show that hexokinase II plays an important role in the hypertrophic response to pressure overload, which is mediated through reactive oxygen species.
Rongxue Wu, Eugene Wyatt, Kusum Chawla, Minh Tran, Mohsen Ghanefar, Markku Laakso, Conrad L. Epting and Hossein Ardehali
EMBO Mol Med 2012, 4(7), 633–646

Cardiac hypertrophy accompanies the majority of disease- and age-related cardiac pathologies. Here, the authors report that miR-142, which targets mediators of growth and survival, ensures that these signals remain quiescent in the non-stressed heart.
Salil Sharma, Jing Liu, Jianqin Wei, Huijun Yuan, Taifang Zhang and Nanette H. Bishopric
EMBO Mol Med 2012, 4(7), 617–632

The authors show that fibronectin plays a dichotomous role in atherosclerosis: it worsens its cause by increasing the atherogenic plaque area but also stabilizes the plaques with fibrous caps and protects from secondary damage and vascular occlusion.
Ina Rohwedder, Eloi Montanez, Karsten Beckmann, Eva Bengtsson, Pontus Dunér, Jan Nilsson, Oliver Soehnlein and Reinhard Fässler
EMBO Mol Med 2012, 4(7), 564–576
Kathryn J. Moore and Edward A. Fisher
EMBO Mol Med 2012, 4(7), 561–563

Here, the authors generated the first human model of catecholaminergic polymorphic ventricular tachycardia (CPVT), an inherited cardiac disease that, under physical and emotional stress, leads to life-threatening arrhythmia.
Christian B. Jung, Alessandra Moretti, Michael Mederos y Schnitzler, Laura Iop, Ursula Storch, Milena Bellin, Tatjana Dorn, Sandra Ruppenthal, Sarah Pfeiffer, Alexander Goedel, Ralf J. Dirschinger, Melchior Seyfarth, Jason T. Lam, Daniel Sinnecker, Thomas Gudermann, Peter Lipp and Karl-Ludwig Laugwitz
EMBO Mol Med 2012, 4(3), 117–119

In this Editorial, Chief Editor Stefanie Dimmeler introduces the Cardiovascular Disease Review Series and stresses the importance of translational research in the field.
Stefanie Dimmeler
EMBO Mol Med 2011, 3(12), 697

In this Perspective, Louis-Jeantet-Prize winner Michel Haïssaguerre describes how he started looking for the origins of atrial fibrillation, a common cardiac arrhythmia that is associated with 350 000 death/year in Europe.
Michel Haïssaguerre
EMBO Mol Med 2010, 2(4), 117–119

In this Review, the authors present their views on the contributions that a systems approach can bring to the study of atherosclerosis, propose ways to tackle the complexity of the disease in a systems manner and review recent systems-level studies of the disease.
Stephen A. Ramsey, Elizabeth S. Gold and Alan Aderem
EMBO Mol Med 2010, 2(3), 79–89

Here, the authors show that SPAK regulates blood pressure by controlling the activity as well as expression of the renal sodium cotransporters NCC and NKCC2.
Fatema H. Rafiqi, Annie Mercier Zuber, Mark Glover, Ciaran Richardson, Stewart Fleming, Sofija Jovanovic, Aleksandar Jovanovic, Kevin M. O'Shaughnessy and Dario R. Alessi
EMBO Mol Med 2010, 2(2), 63-75
María Castañeda-Bueno and Gerardo Gamba
EMBO Mol Med 2010, 2(2), 39–41