Cardiology articles within Nature Communications

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  • Article
    | Open Access

    Myocardial tissue undergoes steady functional decline when cultured in vitro. Here, the authors report a protocol for culture of human cardiac slices that allows maintenance of contractility for up to four months, and show that the model is suitable for evaluation of drug safety, as exemplified for drugs interfering with cardiomyocyte repolarization.

    • Carola Fischer
    • , Hendrik Milting
    •  & Andreas Dendorfer

  • Article
    | Open Access

    Thrombospondin 4 has been shown to protect the heart and the skeletal muscle by enhancing matrix secretion and membrane stability thanks to its intracellular function. Here the authors show that thrombospondin 3 exacerbates injury-induced cardiomyopathy and promotes destabilization of the cardiomyocyte membrane by impairing integrin trafficking to the sarcolemma.

    • Tobias G. Schips
    • , Davy Vanhoutte
    •  & Jeffery D. Molkentin

  • Article
    | Open Access

    Studying the genetic underpinnings of physical activity and sleep duration can be confounded by self-reporting. Here, Doherty et al. use data from 91,105 UK Biobank participants, whose activity had been monitored for a week by a wearable device, for genome-wide association analysis and identify 14 loci.

    • Aiden Doherty
    • , Karl Smith-Byrne
    •  & Cecilia M. Lindgren

  • Article
    | Open Access

    Histone lysine demethylases (KDMs) can mediate transcriptional reprogramming in disease states. Here the authors show that KDM3A promotes left ventricular hypertrophy and cardiac fibrosis by activating the transcription of Timp1, and that pharmacological inhibition of KDM3A attenuates cardiac remodeling induced by pressure overload.

    • Qing-Jun Zhang
    • , Tram Anh T. Tran
    •  & Zhi-Ping Liu

  • Article
    | Open Access

    Blood pressure (BP) is a major risk factor for cardiovascular disease and more than 200 genetic loci associated with BP are known. Here, the authors perform discovery GWAS for BP in East Asians and meta-analysis in East Asians and Europeans and report ancestry-specific BP SNPs and selection signals.

    • Fumihiko Takeuchi
    • , Masato Akiyama
    •  & Norihiro Kato

  • Article
    | Open Access

    Abdominal aortic aneurysms (AAA) are characterized by extensive extracellular matrix degradation. Here Hadi et al. identify a netrin-1/neogenin-based crosstalk between macrophages and vascular smooth muscle cells (VSMCs), leading to the secretion of the matrix metalloproteinase MMP-3 by VSMCs and subsequent matrix degradation in AAA lesions.

    • Tarik Hadi
    • , Ludovic Boytard
    •  & Bhama Ramkhelawon

  • Article
    | Open Access

    Constitutive deletion of Rcan1 has been previously shown to prevent Angiotensin II-induced aneurysm in mice. Here the authors show that tissue-specific inducible deletion of Rcan1 in vascular cell types predisposes to hypertension-mediated aortic rupture, intramural hematoma, and aneurysm, due to increased GSK-3b-mediated activation of ROCK and induction of a hypercontractile phenotype.

    • Silvia Villahoz
    • , Paula Sofía Yunes-Leites
    •  & Miguel R. Campanero

  • Article
    | Open Access

    Optogenetic tools enable precise experimental control of the behaviour of cells. Here, the authors introduce a genetically-encoded two-protein system that enables silencing of excitable cells such as neurons and cardiomyocytes using blue light, and demonstrate its utility both in vitro and In vivo.

    • Yinth Andrea Bernal Sierra
    • , Benjamin R. Rost
    •  & Dietmar Schmitz

  • Article
    | Open Access

    A small percentage of cardiomyocytes (CM) are of neural crest origin but the function of such cells in the adult zebrafish is unclear. Here, the authors identify this CM subpopulation as expressing the Notch ligand jag2b and if deleted in the embryo, cause severe hypertrophic cardiomyopathy in adulthood.

    • Sarah Abdul-Wajid
    • , Bradley L. Demarest
    •  & H. Joseph Yost

  • Article
    | Open Access

    Vascular smooth muscle cell (VSMC) accumulation is associated with cardiovascular disease. Here, the authors combine single-cell RNA sequencing with lineage labelling to profile VSMC heterogeneity in healthy mice. They show that upregulation of Sca1 in a rare VSMC subpopulation marks a cell phenotype that is prevalent in disease.

    • Lina Dobnikar
    • , Annabel L. Taylor
    •  & Helle F. Jørgensen

  • Article
    | Open Access

    The mechanisms underlying the transition from cardiac hypertrophy to heart failure following pressure overload are incompletely understood. Here the authors identify the gene programs encoding the morphological and functional characteristics of cardiomyocytes during the transition from early hypertrophy to heart failure via single-cell transcriptomics, establishing a key role for p53 signalling.

    • Seitaro Nomura
    • , Masahiro Satoh
    •  & Issei Komuro

  • Article
    | Open Access

    The cardiac autonomic nervous system produces various neuropeptides, such as neurokinin substance-P (Sub-P), whose function remains largely unclear. Here, authors show that Sub-P causes a receptor-mediated prolongation of the atrial action potential through a reduced background potassium current, and prevents atrial fibrillation.

    • Marieke W. Veldkamp
    • , Guillaume S. C. Geuzebroek
    •  & Ruben Coronel

  • Article
    | Open Access

    Common genetic variants in structural proteins contribute to risk of atrial fibrillation (AF). Here, using whole-exome sequencing, the authors identify rare truncating variants in TTN that associate with familial and early-onset AF and show defects in cardiac sarcomere assembly in ttn.2-mutant zebrafish.

    • Gustav Ahlberg
    • , Lena Refsgaard
    •  & Morten S. Olesen

  • Article
    | Open Access

    Nitric oxide (NO) inhibits thrombosis in part by stimulating cyclic guanosine monophosphate (cGMP) production and cGMP-dependent protein kinase I (cGKI) activity in platelets. Here, Wen et al. develop a cGMP sensor mouse to follow cGMP dynamics in platelets, and find that shear stress activates NO-cGMP-cGKI signaling during platelet aggregation to limit thrombosis.

    • Lai Wen
    • , Susanne Feil
    •  & Robert Feil

  • Article
    | Open Access

    Due to the limited proliferation capacity of adult mammalian cardiomyocytes, the human heart has negligible regenerative capacity after injury. Here the authors show that a Hedgehog-Gli1-Mycn signaling cascade regulates cardiomyocyte proliferation and cardiac regeneration from amphibians to mammals.

    • Bhairab N. Singh
    • , Naoko Koyano-Nakagawa
    •  & Daniel J. Garry

  • Article
    | Open Access

    Excessive production of reactive oxygen species (ROS) is associated with cardiac dysfunction, but the causal role of ROS remains poorly understood. Here the authors use an in vivo chemogenetic approach to develop a heart failure model in which generation of hydrogen peroxide in the heart leads to systolic heart failure without fibrotic remodeling.

    • Benjamin Steinhorn
    • , Andrea Sorrentino
    •  & Thomas Michel

  • Article
    | Open Access

    Hypertrophic cardiomyopathy (HCM) is caused by point mutations in sarcomeric proteins. Here the authors develop an optimized model of the sequestered state of cardiac myosin and define the features affecting the lever arm compliance, allowing them to group mutations in classes and to elucidate the molecular mechanisms leading to cardiac dysfunction in HCM.

    • Julien Robert-Paganin
    • , Daniel Auguin
    •  & Anne Houdusse

  • Article
    | Open Access

    Common genetic variants associated with plasma lipids have been extensively studied for a better understanding of common diseases. Here, the authors use whole-genome sequencing of 16,324 individuals to analyze rare variant associations and to determine their monogenic and polygenic contribution to lipid traits.

    • Pradeep Natarajan
    • , Gina M. Peloso
    •  & Sebastian Zoellner

  • Article
    | Open Access

    Hypertrophic cardiomyocytes switch their metabolism from fatty acid oxidation to glucose use, but the functional role of this change is unclear. Here the authors show that high intracellular glucose inhibits the degradation of branched-chain amino acids, which is required for the activation of pro-growth mTOR signaling.

    • Dan Shao
    • , Outi Villet
    •  & Rong Tian

  • Article
    | Open Access

    Abnormal PR interval duration is associated with risk for atrial fibrillation and heart block. Here, van Setten et al. identify 44 PR interval loci in a genome-wide association study of over 92,000 individuals and find genetic overlap with QRS duration, heart rate and atrial fibrillation.

    • Jessica van Setten
    • , Jennifer A. Brody
    •  & Nona Sotoodehnia

  • Article
    | Open Access

    MicroRNAs play important roles in endothelial cells injury, proliferation and maladaptation by negatively regulating posttranscriptional gene expression. Here the authors uncover the role of the long non coding RNA lncWDR59, target of miR-103, in endothelial maladaptation.

    • Lucia Natarelli
    • , Claudia Geißler
    •  & Andreas Schober

  • Article
    | Open Access

    Genome-wide association studies have identified multiple loci for resting heart rate (HR) but the genetic factors associated with HR increase during and HR recovery after exercise are less well studied. Here, the authors examine both traits in a two-stage GWAS design in up to 67,257 individuals from UK Biobank.

    • Julia Ramírez
    • , Stefan van Duijvenboden
    •  & Patricia B. Munroe

  • Article
    | Open Access

    The adult mammalian heart has a limited cardiomyogenic capacity. Here the authors show that intensive exercise leads to a 4.6-fold increase in murine cardiomyocyte proliferation requiring the expression of miR-222, and that exercise induces an extended cardiomyogenic response in the murine heart after infarction.

    • Ana Vujic
    • , Carolin Lerchenmüller
    •  & Anthony Rosenzweig

  • Article
    | Open Access

    Cathelicidins are antimicrobial peptides that eliminate pathogens and contribute to the innate immune response. Here the authors show that neutrophil-derived LL-37/CRAMP induces platelet activation and promotes arterial thrombosis and thrombo-inflammation.

    • Joachim Pircher
    • , Thomas Czermak
    •  & Christian Schulz

  • Article
    | Open Access

    Diabetes is associated with an increased thrombotic response, but the mechanism is unknown. Here the authors demonstrate that compressive force activates integrin αIIbβ3 on discoid diabetic platelets and that platelet aggregates can be eliminated by PI 3-kinase inhibition, but not by anti-thrombotics aspirin or clopidogrel.

    • Lining Ju
    • , James D. McFadyen
    •  & Shaun P. Jackson

  • Article
    | Open Access

    Aortic valve stenosis (AS) is the most common valvular heart disease. Here the authors identify two new AS loci that also associate with bicuspid aortic valve, aortic root diameter and/or coronary artery disease implicating both developmental abnormalities and atherosclerosis-like processes in AS.

    • Anna Helgadottir
    • , Gudmar Thorleifsson
    •  & Kari Stefansson

  • Article
    | Open Access

    Response of the heart rate (HR) to exercise is associated with cardiac fitness and risk of cardiac death. Here, in a genome-wide association study, Verweij et al. identify 23 loci for HR increase during exercise or HR recovery, and highlight pleiotropy with blood pressure by polygenic risk score analysis.

    • Niek Verweij
    • , Yordi J. van de Vegte
    •  & Pim van der Harst

  • Article
    | Open Access

    During early postnatal development in mammals, cardiomyocytes exit the cell cycle, losing their regenerative capacity. Here the authors show that, following myocardial infarction, loss of microRNA-128 promotes cardiomyocyte proliferation and cardiac regeneration in adult mice partly via enhancing the expression of the chromatin modifier SUZ12.

    • Wei Huang
    • , Yuliang Feng
    •  & Yigang Wang

  • Article
    | Open Access

    It is not clear if it is the embryonic origin or anatomical location of cardiomyocytes that restrict their contribution to zebrafish heart regeneration. Here, the authors show a plasticity of embryonic precursors following tbx5a fate mapping and that trabecular cardiomyocytes help to rebuild the cortical myocardium.

    • Héctor Sánchez-Iranzo
    • , María Galardi-Castilla
    •  & Nadia Mercader

  • Article
    | Open Access

    Heart development requires compaction of the ventricular wall into a dense myocardium at mid-gestation. Here, Rhee and colleagues show that the chromatin remodeller Ino80 is critical for the formation of the coronary vasculature, and show that coronary vessels are needed for successful cardiac compaction during embryonic development.

    • Siyeon Rhee
    • , Jae I. Chung
    •  & Kristy Red-Horse

  • Article
    | Open Access

    AMPK activation inhibits cardiac hypertrophy. Here the authors show that this occurs independently of previously proposed mechanisms and that AMPK controls the phosphorylation of the aminotransferase GFAT, thereby preventing cardiac hypertrophy through the reduction of protein O-GlcNAcylation.

    • Roselle Gélinas
    • , Florence Mailleux
    •  & Luc Bertrand

  • Article
    | Open Access

    Protein phosphatase 5 (PP5) is expressed in many cell types but its role in cardiomyocytes is unknown. Here the authors show that PP5 binds and dephosphorylates elastic titin in cardiac sarcomeres, and that PP5 is increased in heart failure, reducing cardiomyocyte compliance.

    • Judith Krysiak
    • , Andreas Unger
    •  & Wolfgang A. Linke

  • Article
    | Open Access

    Voltage-gated sodium channels are expressed in excitable tissues and mutations have been linked to cardiac arrhythmias and channelopathies. Here the authors show that the sodium channel α-subunits interact to form a dimer and gate as dimer and that this functional dimerisation is conserved.

    • Jérôme Clatot
    • , Malcolm Hoshi
    •  & Isabelle Deschênes

  • Article
    | Open Access

    Little is known about the changes in mRNA splicing, processing and stability that can alter gene expression during heart failure. Here, the authors show that BEX1 is induced during heart failure and is part of a ribonucleoprotein complex enhancing the expression and stability of proinflammatory genes.

    • Federica Accornero
    • , Tobias G. Schips
    •  & Jeffery D. Molkentin

  • Article
    | Open Access

    Formation of the vascular lumen initiates the blood flow and it is crucial for tissue homeostasis. Here, Li et. al show that the R-Ras-Akt signaling axis is crucial for reparative angiogenesis in mice because it stabilizes the microtubule cytoskeleton in endothelial cells to promote endothelial lumen formation.

    • Fangfei Li
    • , Junko Sawada
    •  & Masanobu Komatsu

  • Article
    | Open Access

    Mutations in potassium and calcium channel genes have been associated with cardiac arrhythmias. Here, Jensen et al. show that an anion transporter chloride-bicarbonate exchanger AE3 is also responsible for the genetically-induced mechanism of cardiac arrhythmia, suggesting new therapeutic targets for this disease

    • Kasper Thorsen
    • , Vibeke S. Dam
    •  & Henrik K. Jensen

  • Article
    | Open Access

    Pericytes are essential for the development, maintenance and function of vascular networks. Here, Eilken and colleagues show that expression of the decoy receptor VEGFR1 by pericytes spatially restricts VEGF signalling, thus regulating VEGF-induced endothelial cell sprouting in developing tissues.

    • Hanna M. Eilken
    • , Rodrigo Diéguez-Hurtado
    •  & Ralf H. Adams

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