Ventricular fibrillation articles within Nature Communications

Featured

• Article
  10 January 2022 | Open Access

  Synthetic recovery of impulse propagation in myocardial infarction via silicon carbide semiconductive nanowires

  Silicon-based materials have the ability to support bioelectrical activity. Here the authors show how injectable silicon carbide nanowires reduce arrhythmias and rapidly restore conduction in a myocardial infarction model.

  • Paola Lagonegro
  • , Stefano Rossi
  •  & Michele Miragoli

• Article
  05 February 2021 | Open Access

  Pathological conformations of disease mutant Ryanodine Receptors revealed by cryo-EM

  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
  22 November 2017 | Open Access

  Loss-of-activity-mutation in the cardiac chloride-bicarbonate exchanger AE3 causes short QT syndrome

  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
  24 July 2017 | Open Access

  Plakophilin-2 is required for transcription of genes that control calcium cycling and cardiac rhythm

  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
  27 January 2017 | Open Access

  Disruption of cardiac cholinergic neurons enhances susceptibility to ventricular arrhythmias

  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
  04 October 2016 | Open Access

  Fhf2 gene deletion causes temperature-sensitive cardiac conduction failure

  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 | 14 August 2014

  Carbon monoxide inhibits inward rectifier potassium channels in cardiomyocytes

  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