Acute coronary syndromes articles within Nature

Featured

  • Article |

    A time-resolved high-resolution map of human cardiac remodelling after myocardial infarction, integrating single-cell transcriptomic, chromatin accessibility and spatial transcriptomic data, provides a valuable resource for the field.

    • Christoph Kuppe
    • , Ricardo O. Ramirez Flores
    •  & Rafael Kramann

  • Outlook |

    New imaging methods and biomarkers may help identify people who are at risk for heart disease but are overlooked by standard risk assessments.

    • Peter Gwynne

  • Article |

    The human heart regenerates poorly, causing insufficient healing after injury; here, microRNAs screened for the ability to induce cardiomyocyte proliferation are shown to stimulate cardiac regeneration and almost complete recovery of the heart after infarction.

    • Ana Eulalio
    • , Miguel Mano
    •  & Mauro Giacca

  • Letter |

    During normal ageing a low rate of division of pre-existing cardiomyocytes, rather than progenitor cells, is responsible for cardiomyocyte genesis; this process is increased fourfold during myocardial infarction.

    • Samuel E. Senyo
    • , Matthew L. Steinhauser
    •  & Richard T. Lee

  • News & Views |

    Heart attacks occur when lipoprotein-driven inflammation called atherosclerosis triggers blood clotting in the arteries. It seems that the attacks can, in turn, accelerate atherosclerosis by fanning the inflammation. See Letter p.325

    • Ira Tabas

  • Article |

    Myocardial infarction accelerates atherosclerosis through activation of the sympathetic nervous system, and the consequent release of haematopoietic stem and progenitor cells.

    • Partha Dutta
    • , Gabriel Courties
    •  & Matthias Nahrendorf

  • Article |

    A combination of four transcription factors, GATA4, HAND2, MEF2C and TBX5, can reprogram fibroblasts into cardiac-like myocytes in vitro and in vivo; expression of these factors ameliorated cardiac function in mice that had suffered myocardial infarction.

    • Kunhua Song
    • , Young-Jae Nam
    •  & Eric N. Olson

  • Article |

    A non-coding polymorphism at a locus associated with myocardial infarction in humans creates a CCAAT/enhancer binding protein transcription factor binding site and alters the hepatic expression of the SORT1 gene. These authors show that modulating Sort1 levels in mouse liver alters levels of plasma low-density lipoprotein cholesterol and very low-density lipoprotein, potentially explaining why polymorphisms at this locus are associated with heart disease.

    • Kiran Musunuru
    • , Alanna Strong
    •  & Daniel J. Rader

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