Cardiovascular diseases articles within Nature

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  • 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

  • Article |

    This study shows that cardiac injury induces cardiac fibroblasts to undergo mesenchymal–endothelial transition and acquire an endothelial-cell like fate, a process mediated, in part, by a p53-dependent mechanism — use of a small molecule activator of p53 increases mesenchymal–endothelial transition, leading to reduced scarring and better preservation of heart function.

    • Eric Ubil
    • , Jinzhu Duan
    •  & Arjun Deb

  • Letter |

    Here, a long noncoding RNA, termed Mhrt, is identified in the loci of myosin heavy chain (Myh) genes in mice and shown to be capable of suppressing cardiomyopathy in the animals, as well as being repressed in diseased human hearts.

    • Pei Han
    • , Wei Li
    •  & Ching-Pin Chang

  • Letter |

    During development of myointimal hyperplasia in human arteries, smooth muscle cells have hyperpolarized mitochondrial membrane potential (ΔΨm), high proliferation and apoptosis resistance; PDK2 is a key regulatory protein whose activation is necessary for myointima formation, and its blockade with dichloroacetate prevents Δψm hyperpolarization, facilitates apoptosis and reduces myointima formation in injured arteries, without preventing vessel re-endothelialization, possibly representing a novel strategy to prevent proliferative vascular diseases.

    • Tobias Deuse
    • , Xiaoqin Hua
    •  & Sonja Schrepfer

  • 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

  • Letter |

    A role is demonstrated for miR-34a, a microRNA that is upregulated in the ageing heart; miR-34a downregulates PNUTS, a protein that protects cardiomyocytes and telomeres, silencing of miR-34a is therefore a promising therapeutic target.

    • Reinier A. Boon
    • , Kazuma Iekushi
    •  & Stefanie Dimmeler

  • 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

  • Outlook |

    New drugs and more focused therapy might cut down on atrial fibrillation and reduce the incidence of stroke.

    • Neil Savage

  • Outlook |

    The standard medications for hypertension and cholesterol have lingering issues, but new drugs hold promise for high-risk patients.

    • Katharine Gammon

  • Outlook |

    Mental factors beyond stress trigger physiological changes that can cause heart disease.

    • Shailaja Neelakantan

  • Outlook |

    Better thought-out town planning and interior design can create healthier environments, but how to effectively implement the best designs remains uncertain.

    • Duncan Graham-Rowe

  • Outlook |

    A hormone system adapted for self-preservation can break and fix your heart, say Sébastien Foulquier, Ulrike Muscha Steckelings and Thomas Unger.

    • Sébastien Foulquier
    • , Ulrike Muscha Steckelings
    •  & Thomas Unger

  • Outlook |

    Severe psoriasis carries cardiovascular risks. Dermatologists should consider more than just patients' outer layers, argues Henning Boehncke.

    • Wolf-Henning Boehncke

  • 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

  • Q&A |

    Cardiologist is first winner of award supporting clinical research.

    • Charlotte Schubert

  • Letter |

    A guinea-pig model of cardiac injury is used to show that human embryonic stem-cell-derived cardiomyocyte grafts can electrically integrate into the injured heart, improving mechanical function and reducing spontaneous and induced ventricular tachycardia; this is a major step towards clinical adoption of cell replacement therapies for cardiovascular diseases using human cardiomyocytes.

    • Yuji Shiba
    • , Sarah Fernandes
    •  & Michael A. Laflamme

  • 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

  • Letter |

    APJ is shown to be a bifunctional receptor for both mechanical stretch and the endogenous peptide apelin, a finding that is important for the development of APJ agonists to treat heart failure.

    • Maria Cecilia Scimia
    • , Cecilia Hurtado
    •  & Pilar Ruiz-Lozano

  • 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

  • News & Views |

    When the heart is injured, the muscle does not regenerate and scars are produced. This process can be attenuated in the hearts of live mice by forcing scar-forming cells to become muscle cells. See Articles p.593 & p.599

    • Nathan J. Palpant
    •  & Charles E. Murry

  • 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

  • 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

  • Article |

    Evidence from mice and humans indicates that peripartum cardiomyopathy (PPCM) is a vascular disease caused by excessive anti-angiogenic signalling in the peripartum period of pregnancy and that pre-eclampsia and multiple gestation are important risk factors for the development of PPCM.

    • Ian S. Patten
    • , Sarosh Rana
    •  & Zoltan Arany

  • Letter |

    Pregnant corin- or ANP-deficient mice have impaired trophoblast invasion and uterine spiral artery remodelling, and patients with pre-eclampsia have lower uterine corin messenger RNA and protein levels than normal pregnancies, suggesting that defects in corin and ANP function may contribute to pre-eclampsia.

    • Yujie Cui
    • , Wei Wang
    •  & Qingyu Wu

  • 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

  • Letter |

    Circadian rhythmicity of cardiac ion-channel expression and of an index of myocardial repolarization is under the control of Klf15, a clock-dependent oscillator that is required for generating transient outward potassium current, and deficiencies or excesses of which cause loss of rhythmic variation in myocardial and abnormal repolarization, and an enhanced susceptibility to ventricular arrhythmias.

    • Darwin Jeyaraj
    • , Saptarsi M. Haldar
    •  & Mukesh K. Jain

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