Image courtesy of Megan Farrell and Arianne Caudal

Read our September issue

The age-dependent sex differences in cardiometabolic risk factors, the metabolic defects in failing human hearts, the cre toxicity in cardiovascular mouse models and much more!   

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  • Destici, Zhu, et al. identify human-specific cis-regulatory elements (CREs) through a comparative epigenomic analysis of human and mouse cardiomyocytes at early stage of development and show that these CREs could contribute to species-specific cardiac features. Human-specific enhancers were particularly enriched in SNPs associated with human-specific traits (such as increased heart resting rate, atrial fibrillation and QRS duration), and the acquisition of human-specific enhancers could expand the functionality of the conserved transcriptional regulator ZIC3 by modifying its spatio-temporal expression.

    • Eugin Destici
    • Fugui Zhu
    • Neil C. Chi
    Article
  • With the use of the Lifelines cohort, Zhernakova and colleagues set out to characterize sex differences in cardiometabolic risk factors, metabolites and proteins in adults aged 20–80 years and find a strong age effect on sex differences in cardiometabolic disease risk factors and biomarkers.

    • Daria V. Zhernakova
    • Trishla Sinha
    • Jingyuan Fu
    Article Open Access
  • Anbazhakan et al. use whole-organ imaging and three-dimensional computational fluid dynamics modeling to define spatial architecture and predict blood flow through collaterals in neonate and adult mouse hearts after injury, and compare their findings to the functionality of collaterals in human adult and fetal hearts.

    • Suhaas Anbazhakan
    • Pamela E. Rios Coronado
    • Kristy Red Horse
    Article
  • Ngwenyama et al. show that cardiac fibroblasts express MHCII during cardiac inflammation, and are able to process extracellular proteins into small peptides that induce CD4+ T cell immune responses. Conditional deletion of MHCII in cardiac fibroblasts ameliorates cardiac remodeling and dysfunction induced by cardiac pressure overload, supporting a central role for cardiac fibroblast MHCII in antigen presentation and in cardiac fibrosis and dysfunction in experimental HF.

    • Njabulo Ngwenyama
    • Kuljeet Kaur
    • Pilar Alcaide
    Article