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Showing 1–8 of 8 results
Advanced filters: Author: Saptarsi M Haldar Clear advanced filters

  • Despite imaging advances, diagnosis of infective endocarditis is not simple, and uncertainty about whether a surgical or nonsurgical approach is best and the timing of intervention can hamper therapy. In this Review, Saptarsi Haldar and Patrick O'Gara discuss the major features of diagnosis and therapy and make recommendations based on the available data.

    • Saptarsi M Haldar
    • Patrick T O'Gara
    Reviews
    Nature Clinical Practice Cardiovascular Medicine
    Volume: 3, P: 310-317

  • In this study, Hsu et al. show that inhibition of CDK7/12/13 attenuates maladaptive transcriptional activation in cultured cardiomyocytes and a mouse model of heart failure, suggesting that targeting the transcription machinery might be a therapeutic approach to treat heart failure with reduced ejection fraction.

    • Austin Hsu
    • Qiming Duan
    • Saptarsi M. Haldar
    ResearchOpen Access
    Nature Communications
    Volume: 13, P: 1-11

  • Genes encode risk for coronary disease, identifying how they function is critical to developing new therapies. In work reported the authors have identified one culprit gene, PDGFD, and studied how it functions to promote disease risk.

    • Hyun-Jung Kim
    • Paul Cheng
    • Thomas Quertermous
    ResearchOpen Access
    Nature Communications
    Volume: 14, P: 1-17

  • By performing a genome-wide CRISPR screen in human induced pluripotent stem cells, Padmanabhan et al. identify the acetyl-lysine reader protein BRD4 as a regulator of cardiomyocyte differentiation, and they validate in vivo that BRD4 is required during development for the fate determination of a subset of secondary heart field cardiac progenitor cells.

    • Arun Padmanabhan
    • T. Yvanka de Soysa
    • Rajan Jain
    Research
    Nature Cardiovascular Research
    Volume: 3, P: 317-331

  • 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
    Research
    Nature
    Volume: 483, P: 96-99