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  • Song and colleagues show that FDA-approved cough suppressant dextromethorphan could be used as an agonist of sigma non-opioid intracellular receptor 1 (SIGMAR1) to normalize the action potential in human cellular models and a mouse model of Timothy syndrome, a congenital disease with no available treatment. The researchers also show that dextromethorphan normalizes the action potential in human cellular models of two additional inherited cardiac arrhythmias: long QT syndrome types 1 and 2, which are caused by mutations in different genes.

    • LouJin Song
    • Ramsey Bekdash
    • Masayuki Yazawa
    Article
  • Using large-scale single-nucleus transcriptomics, Nicin et al. report insights into human cardiac hypertrophy, caused by pressure overload, at single-cell resolution. The authors show that intercellular communication, particularly via the Eph receptor tyrosine kinase EPHB1, is impaired in human cardiomyopathy.

    • Luka Nicin
    • Sam Michael Schroeter
    • Stefanie Dimmeler
    ResourceOpen Access
  • Honigberg and colleagues analyzed the frequency of depressed mood in conjunction with polygenic risk scores for coronary artery disease (CAD), type 2 diabetes (T2D) and atrial fibrillation in the UK Biobank and showed that depressed mood was independently associated with a lower risk of CAD and T2D across the cardiometabolic polygenic risk spectrum.

    • Michael C. Honigberg
    • Yixuan Ye
    • Pradeep Natarajan
    Letter
  • Koplev et al. apply interactive system analyses to infer and characterize gene-regulatory networks (GRNs) active within and across tissues that cause cardiometabolic disease and coronary artery disease (CAD). By including GWAS in the integrative analysis, the provided multiorgan framework of GRNs is suggested to explain significantly more heritability of CAD than what has been achieved by analyzing GWAS alone.

    • Simon Koplev
    • Marcus Seldin
    • Johan L. M. Björkegren
    Article
  • Sick heart and vessels skew hematopoiesis toward inflammatory myeloid cells. Rhode et al. show that hypertension, atherosclerosis and myocardial infarction cause endothelial dysfunction in bone marrow (BM), which in return causes overproduction of inflammatory myeloid cells and systemic leukocytosis in mice. This process is mediated by VEGF signaling, IL-6 and versican production by the BM endothelium.

    • David Rohde
    • Katrien Vandoorne
    • Matthias Nahrendorf
    ArticleOpen Access