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!

Announcements

  • https://career5.successfactors.eu/sfcareer/jobreqcareer?jobId=38221&company=C0001215517P

    Do you have strong background in cardiovascular or hematology research, a passion for science and a thirst to learn more? Would you like to help shape a new scientific journal that will serve scientist across all disciplines of cardiovascular and hematology research? If the answer to these questions is "yes", click on the image to apply for the job and join our team!

  • Drawing of an hearth tissue

    Interested in meeting our Editors for a lab or site visit? Click the link above to learn more.

Nature Cardiovascular Research is a Transformative Journal; authors can publish using the traditional publishing route OR via immediate gold Open Access.

Our Open Access option complies with funder and institutional requirements.

Advertisement

  • 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
    Article
  • 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
    Letter
  • 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
    Article
  • 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
    Article
  • 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
    Article