Arrhythmias articles within Nature Communications

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  • Article
    | Open Access

    Electromechanical characterization during atrial fibrillation (AF) remains a significant gap in the understanding of AF-related atrial myopathy. Here, the authors use non-invasive atrial electromechanical assessment during AF to identify early remodeling changes associated with underlying myopathy, which in the clinic decrease the probability of acute and mid-term successful rhythm control.

    • Daniel Enríquez-Vázquez
    • , Jorge G. Quintanilla
    •  & David Filgueiras-Rama

  • Article
    | Open Access

    The intercalated disc (ICD) is a membrane structure of the cardiac muscle involved in normal heart function. Here the authors report that knockdown of the ICD-bound transmembrane protein 65 results in impaired ICD structure, abnormal cardiac electrophysiology and cardiomyopathy in mice.

    • Allen C. T. Teng
    • , Liyang Gu
    •  & Anthony O. Gramolini

  • Article
    | Open Access

    Gq proteins are one of four major classes of G proteins; optogenetic receptors for selective and repetitive activation of Gq proteins with fast kinetics are lacking. Here the authors report UV light-dependent Gq signalling using human Neuropsin (hOPN5) and demonstrate its potential as an optogenetic tool.

    • Ahmed Wagdi
    • , Daniela Malan
    •  & Tobias Bruegmann

  • Article
    | Open Access

    An abnormal cardiac action potential underlies different types of cardiac arrhythmias. Here the authors show that microRNA-365 regulates the cardiac action potential by modulating key cardiac repolarizing channels.

    • Dena Esfandyari
    • , Bio Maria Ghéo Idrissou
    •  & Stefan Engelhardt

  • Article
    | Open Access

    Noninvasive cardiac radiotherapy may effectively manage ventricular tachycardia in refractory patients, but its radiobiologic mechanisms of action are unclear. Here, the authors show that photon radiation durably and favourably reprograms cardiac conduction in the absence of transmural fibrosis suggesting this could be the mechanism through which cardiac radiotherapy to modulates arrhythmia susceptibility.

    • David M. Zhang
    • , Rachita Navara
    •  & Stacey L. Rentschler

  • Article
    | Open Access

    Cardiac function fluctuates greatly across the day and night, but this is not simply a consequence of our changing behaviour. The authors highlight the role of the body’s circadian clock in regulating the heart electrical activity, including a time-of-day dependent susceptibility to cardiac arrhythmias.

    • Edward A. Hayter
    • , Sophie M. T. Wehrens
    •  & David A. Bechtold

  • Article
    | Open Access

    Cardiac immune cells play various roles in the maintenance of homeostasis and diseases in the heart. Here the authors show that cardiac resident macrophages are a critical regulator of cardiac impulse conduction through amphiregulin production, contributing to the prevention of sudden death.

    • Junichi Sugita
    • , Katsuhito Fujiu
    •  & Issei Komuro

  • Article
    | Open Access

    Ryanodine Receptors (RyRs) release Ca2+ from the endoplasmic and sarcoplasmic reticulum. Mutations in RyR are linked to malignant hyperthermia (MH), myopathies, and arrhythmias. Here, a collection of cryoEM structures provides insights into the molecular consequences of MHrelated RyR mutation R615C, and how apoCaM opens RyR1.

    • Kellie A. Woll
    • , Omid Haji-Ghassemi
    •  & Filip Van Petegem

  • Article
    | Open Access

    The involvement of cAMP-dependent regulation of HCN4 in the chronotropic heart rate response is a matter of debate. Here the authors use a knockin mouse model expressing cAMP-insensitive HCN4 channels to discover an inhibitory nonfiring cell pool in the sinoatrial node and a tonic and mutual interaction between firing and nonfiring pacemaker cells that is controlled by cAMP-dependent regulation of HCN4, with implications in chronotropic heart rate responses.

    • Stefanie Fenske
    • , Konstantin Hennis
    •  & Christian Wahl-Schott

  • Article
    | Open Access

    The role of of voltage-gated sodium channels (Nav) in pacemaking and conduction of the human sinoatrial node is unclear. Here, the authors investigate existence and function of neuronal and cardiac Nav in human sinoatrial nodes, and demonstrate their alterations in explanted human diseased hearts.

    • Ning Li
    • , Anuradha Kalyanasundaram
    •  & Vadim V. Fedorov

  • Article
    | Open Access

    The depolarizing funny current contributing to cardiac pacemaking is upregulated in the myocardium of  failing and infarcted hearts, but whether the current is implied in disease mechanisms is unclear. Here the authors generate HCN4 transgenic mice and show that upregulation of funny current to the levels observed in human heart failure alters calcium homeostasis leading to cardiac remodelling and arrhythmia.

    • Pessah Yampolsky
    • , Michael Koenen
    •  & Patrick A. Schweizer

  • Article
    | Open Access

    Atrial fibrillation (AF) is accompanied by a detrimental loss of functional cardiomyocytes. Here, Zhang et al. show that AF-induced cardiomyocyte dysfunction is a consequence of DNA damage-mediated PARP1 activation, which leads to depletion of NAD+ and further oxidative stress and DNA damage, and identify PARP1 inhibition as a potential therapeutic strategy in the treatment of AF.

    • Deli Zhang
    • , Xu Hu
    •  & Bianca J. J. M. Brundel

  • 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

    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

    KCNQ1 is a voltage-gated potassium channel that is important in cardiac and epithelial function. Here the authors present a mechanism for KCNQ1 activation and inactivation in which voltage sensor activation promotes pore opening more effectively in the intermediate open state than the fully open state, generating inactivation.

    • Panpan Hou
    • , Jodene Eldstrom
    •  & Jianmin Cui

  • 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

    The human heart is composed of distinct regions and cell types, but relatively little is known about their specific protein composition. Here, the authors present a region- and cell type-specific proteomic map of the healthy human heart, revealing functional differences and potential cell type markers.

    • Sophia Doll
    • , Martina Dreßen
    •  & Matthias Mann

  • Article
    | Open Access

    It is believed that mutations in desmosomal adhesion complex protein plakophilin 2 (PKP2) cause arrhythmia due to loss of cell-cell communication. Here the authors show that PKP2 controls the expression of proteins involved in calcium cycling in adult mouse hearts, and that lack of PKP2 can cause arrhythmia in a structurally normal heart.

    • Marina Cerrone
    • , Jerome Montnach
    •  & Mario Delmar

  • Article
    | Open Access

    Catheter ablation is a common therapy for atrial fibrillation but disrupts cardiac cholinergic neurons. Here the authors report that cholinergic neurons innervate heart ventricles and show that their ablation leads to increased susceptibility to ventricular arrhythmias in mouse models and in patients.

    • Christiane Jungen
    • , Katharina Scherschel
    •  & Christian Meyer

  • Article
    | Open Access

    Ventricular arrhythmia is a leading cause of death in patients with diabetes. Here the authors show that inflammasome activation and ILK-1β production in cardiac macrophages cause arrhythmia in diabetic mice, which can be successfully treated using agonists to IL-1β receptor or NLRP3 inhibitors.

    • Gustavo Monnerat
    • , Micaela L. Alarcón
    •  & Emiliano Medei

  • Article
    | Open Access

    Fever is a defence mechanism against infection, but it may also cause abnormal heart rhythm viaunknown mechanism. Here the authors identify FHF2 protein as a key regulator of myocardial excitability that protects the heart against conduction failure in response to an increase in body temperature.

    • David S. Park
    • , Akshay Shekhar
    •  & Glenn I. Fishman

  • Article
    | Open Access

    Cardiac voltage-gated sodium channels (Nav1.5) are crucial regulators of heart electric activity. Here the authors show that palmitoylation, a process of lipid modification of cysteine residues, modulates Nav1.5 function and affects cardiomyocyte excitability, representing a potential target in treating cardiac diseases.

    • Zifan Pei
    • , Yucheng Xiao
    •  & Theodore R. Cummins

  • Article
    | Open Access

    Sudden arrhythmic death is a leading cause of mortality, however approaches to identify at-risk patients are of low sensitivity and specificity. Here, the authors develop a personalized approach to assess arrhythmia risk in post-infarction patients based on cardiac imaging and computational modelling that significantly outperforms existing clinical metrics.

    • Hermenegild J. Arevalo
    • , Fijoy Vadakkumpadan
    •  & Natalia A. Trayanova

  • Article
    | Open Access

    Here, Michael Gollob and colleagues perform a whole exome sequencing study to identify a mutation in the atrial-specific myosin light chain gene MYL4 in a small family with autosomal dominant familial atrial fibrillation. They also test the functionality of this MYL4mutation in zebrafish cardiac function and recapitulate disease-related phenotypes.

    • Nathan Orr
    • , Rima Arnaout
    •  & Michael H. Gollob

  • Article
    | Open Access

    Tsai et al. here utilize a multi-stage genome-wide association study in Taiwanese population to show a copy number variation in the intron of potassium interacting channel 1 gene (KCNIP1) to be strongly associated with atrial fibrillation. The study also examines the functionality of KCNIP1 in heart electrophysiological function using cultured myocytes and zebrafish.

    • Chia-Ti Tsai
    • , Chia-Shan Hsieh
    •  & Jiunn-Lee Lin

  • Article
    | Open Access

    Timothy Syndrome (TS) is a multisystem disorder caused by two mutations leading to dysfunction of the CaV1.2 channel. Here, Dick et al. uncover a major and mechanistically divergent effect of both mutations on Ca2+/calmodulin-dependent inactivation of CaV1.2 channels, suggesting genetic variant-tailored therapy for TS treatment.

    • Ivy E. Dick
    • , Rosy Joshi-Mukherjee
    •  & David T. Yue

  • Article |

    Mechanical and electrical activity in the heart is propagated through unique cardiomyocyte membrane structures, the intercalated discs (ID). Sharma et al.identify a novel ID protein, Tmem65, that controls Ca2+ signalling and electrical coupling by interacting with and functionally regulating the gap junction protein Cx43.

    • Parveen Sharma
    • , Cynthia Abbasi
    •  & Anthony O. Gramolini

  • Article
    | Open Access

    Chondroitin sulfate proteoglycans (CSP) in the myocardial scar inhibit the tissue’s reinnervation, rendering it prone to arrhythmia. Here the authors show that blocking the activity of the CSP receptor, protein tyrosine phosphatase receptor σ, promotes scar reinnervation and prevents arrhythmia in mice.

    • R. T. Gardner
    • , L. Wang
    •  & B. A. Habecker

  • Article |

    Type 2 Long QT syndrome is a cardiac disease associated with hundreds of individual mutations within the Kv11.1 potassium channel. Here, the authors systematically investigate the trafficking defects associated with different types of Kv11.1 mutations and to what extent they can be corrected pharmacologically.

    • Corey L. Anderson
    • , Catherine E. Kuzmicki
    •  & Craig T. January

  • Article |

    Following myocardial infarction, patients are at risk for reperfusion-induced ventricular fibrillation, a life-threatening condition. Here, Liang et al. show that the known ventricular fibrillation preventive effects of carbon monoxide are mediated through the inhibition of a subset of inward-rectifying potassium channels.

    • Shenghui Liang
    • , Quanyi Wang
    •  & Yuchun Gu

  • Article
    | Open Access

    Endurance athletes are known to have a low resting heart rate. Here, D'Souza et al.propose that training-induced bradycardia is the result of electrophysiological changes in the sinus node, challenging the classical view that training-induced bradycardia is caused by increased activity of the autonomic nervous system.

    • Alicia D’Souza
    • , Annalisa Bucchi
    •  & Mark R. Boyett

  • Article |

    Perturbation of the cardiac voltage-gated sodium channel, NaV1.5, by drugs or inherited mutation can underlie and trigger cardiac arrhythmias. Here, the role of the NaV1.5 carboxy terminus in channel inactivation is investigated, and structural details of an arrhythmia associated H6 mutant are reported.

    • Ian W. Glaaser
    • , Jeremiah D. Osteen
    •  & Robert S. Kass

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