Image courtesy of Cornelia Weyand, Tuantuan Zhao, Mayo Clinic

Read our July issue

The opposing effect of macrophages and neutrophils on ventricular arrhythmia after myocardial infarction, how coronary artery disease affects the anti-viral response, how IgE promotes PAH, and more!



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  • Su, Chen et al. show that sepsis-derived S100A8/A9 induces GSDMD-dependent platelet pyroptosis via the TLR4/ROS/NLRP3/caspase 1 pathway, leading to the release of ox-mtDNA contributing to neutrophil extracellular traps (NET) formation. NET in turn release S100A8/A9 and accelerate platelet pyroptosis, forming a positive feedback loop, thereby amplifying the production of proinflammatory cytokines. GSDMD deficiency in platelets or pharmacological inhibition of S100A9 using Paquinimod can break this detrimental feedback loop, thus ameliorating excessive NET-mediated inflammation in mouse models of severe sepsis.

    • Meiling Su
    • Chaofei Chen
    • Wai Ho Tang
  • Using data from the MONICA/KORA registry, Chen et al. show that the risk of heat-related non-fatal myocardial infarction was significantly elevated in patients receiving anti-platelet medication and beta-receptor blockers compared with non-users, and the effect of the medications was stronger in younger patients, with lower prevalence of pre-existing cardiovascular disease, compared with older patients.

    • Kai Chen
    • Robert Dubrow
    • Alexandra Schneider
  • Lam et al. show that conditional deletion of calcineurin B1 in cardiomyocytes and its inhibition using the US Food and Drug Administration-approved drug, FK506, promotes cardiomyocyte cell-cycle re-entry and increases cardiomyocyte numbers in adult mice

    • Nicholas T. Lam
    • Ngoc Uyen Nhi Nguyen
    • Hesham A. Sadek
  • Zhao et al. show that, in patients with coronary artery disease, CD4+ T cells present a blunted response to SARS-CoV-2 and Epstein–Barr viral antigens, due to the overexpression of the immune checkpoint CD155 in macrophages, primed by the exposure to low-density lipoprotein and its oxidized form. The experiments show that CD155 overexpression is due to stabilizing post-translational modifications mediated by the mRNA methylase MTTL3.

    • Tuantuan V. Zhao
    • Zhaolan Hu
    • Cornelia M. Weyand
  • Grune et al. show that hypokalemic mice develop spontaneous ventricular tachycardia after myocardial infarction, and they use this model to dissect the role of immune cells in arrhythmia: neutrophils increase ventricular tachycardia, partly by promoting reactive oxygen species production, whereas efferocytic macrophages play a protective role.

    • Jana Grune
    • Andrew J. M. Lewis
    • Matthias Nahrendorf
    Article Open Access
  • Using rat and mouse models of pulmonary hypertension and patients’ data, Shu, Liu, Zhou et al. show that the concomitant increase in immunoglobulin E (IgE) and mast cells expressing the effector receptor FcεRIα has an important role in pulmonary vascular remodeling, and genetic and pharmacological inhibition of the IgE–FcεRIα signaling alleviated the progression of pulmonary hypertension in animal models.

    • Ting Shu
    • Ying Liu
    • Chen Wang