Heart failure articles within Nature

Featured

  • Article |

    MARK4 regulates cardiomyocyte contractility by promoting MAP4 phosphorylation, which facilitates the access of VASH2 to microtubules for the detyrosination of α-tubulin; MARK4 deficiency after acute myocardial infarction limits the reduction in the left ventricular ejection fraction.

    • Xian Yu
    • , Xiao Chen
    •  & Xuan Li

  • Article |

    A genome-wide association study shows that myocardial trabeculae are an important determinant of cardiac performance in the adult heart, identifies conserved pathways that regulate structural complexity and reveals the influence of trabeculae on the susceptibility to cardiovascular disease.

    • Hannah V. Meyer
    • , Timothy J. W. Dawes
    •  & Declan P. O’Regan

  • Article |

    Cardiac stem cell therapy in mouse models of ischaemia–reperfusion injury demonstrates that improvement in heart function is linked to an immune response characterized by the induction of CCR2+ and CX3CR1+ macrophages.

    • Ronald J. Vagnozzi
    • , Marjorie Maillet
    •  & Jeffery D. Molkentin

  • Letter |

    Adoptive transfer of CAR T cells against the fibroblast marker FAP reduces cardiac fibrosis and restores function after cardiac injury in mice, providing proof-of-principle for the development of immunotherapeutic treatments for cardiac disease.

    • Haig Aghajanian
    • , Toru Kimura
    •  & Jonathan A. Epstein

  • Article |

    iNOS-driven dysregulation of the IRE1α–XBP1 pathway leads to cardiomyocyte dysfunction in mice and recapitulates the systemic and cardiovascular features of human heart failure with preserved ejection fraction.

    • Gabriele G. Schiattarella
    • , Francisco Altamirano
    •  & Joseph A. Hill

  • Letter |

    α1,3-galactosyltransferase-knockout pig hearts that express human CD46 and human thrombomodulin require non-ischaemic preservation with continuous perfusion and post-transplantation growth control to ensure long-term orthotopic function of the xenograft in baboons.

    • Matthias Längin
    • , Tanja Mayr
    •  & Jan-Michael Abicht

  • Letter |

    Deletion of the Hippo pathway component Salvador in mouse hearts with established ischaemic heart failure after myocardial infarction induces a reparative genetic program with increased scar border vascularity, reduced fibrosis, and recovery of pumping function.

    • John P. Leach
    • , Todd Heallen
    •  & James F. Martin

  • Article |

    Myocardial hypoxia activates HIF1α, which activates the splicing factor SF3B1, which mediates a splice switch of the fructose-metabolising enzyme KHK, so that the C isoform that has superior affinity for fructose is expressed in the heart—pathological heart growth and contractile dysfunction can therefore be suppressed by depleting SF3B1 or deleting KHK.

    • Peter Mirtschink
    • , Jaya Krishnan
    •  & Wilhelm Krek

  • Letter |

    Reduced activity of the calcium-transporting ATPase SERCA2a is a hallmark of heart failure; here, microRNAs that downregulate SERCA2a function are identified, and antagonism of one, miR-25, is shown to halt heart failure in mice.

    • Christine Wahlquist
    • , Dongtak Jeong
    •  & Mark Mercola

  • News & Views |

    High blood pressure can damage heart muscle cells and their mitochondrial organelles. DNA from degraded mitochondria has been shown to trigger inflammation leading to heart failure. See Letter p.251

    • Klitos Konstantinidis
    •  & Richard N. Kitsis

  • News & Views |

    Genetic mutations can cause a type of heart disease called dilated cardiomyopathy, by predisposing the organ to enlarge and function poorly. It has now been found that 27% of cases are due to mutations that disrupt the muscle protein titin.

    • Elizabeth M. McNally

  • News & Views |

    Mishandling of calcium ions by cardiac cells causes the heart to malfunction. The discovery of a crucial modification to a calcium pump inside the cell opens up a potential way to correct this. See Letter p.601

    • Sudha K. Shenoy
    •  & Howard A. Rockman

  • News & Views |

    When cardiac muscle cells die during a heart attack, this can lead to heart failure and even death. It now emerges that stem cells of the 'sheet' enveloping the heart can be coaxed to form new muscle after such an event. See Letter p.640

    • Vincent Christoffels

  • News & Views |

    Heart failure is characterized by weakened contractions of heart muscle. A drug that directly activates the key force-generating molecule in this muscle may be a valuable tool to strengthen the failing heart.

    • Donald M. Bers
    •  & Samantha P. Harris

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