Image courtesy of Suhaas Anbazhakan and Pamela E. Rios Coronado

Read our August issue

The cardiac fibroblasts antigen presentation in HF, the effect of heat exposure and medication on MI, the interplay among platelets and NETs in sepsis, the cardiac allo- and xenotransplants and more!



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  • 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
  • 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
  • Through a combination of transcriptomic and proteomic profiling of human right ventricle tissue with plasma proteome profiling in a Canadian cohort of patients with pulmonary arterial hypertension (PAH), Bonnet et al. discovered new circulating proteins associated with right ventricular dysfunction in the setting of PAH.

    • Olivier Boucherat
    • Tetsuro Yokokawa
    • Sebastien Bonnet
  • 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
  • Disease susceptibility and responsiveness to treatment vary among individuals. To understand this diversity, it is crucial to investigate clinical materials and information from large sets of individuals, such as data that can be obtained from biobanks. BioBank Japan is one of the largest biobanks in East Asia and has a complementary role to biobanks from other populations, such as the UK Biobank, given the presence of diverse ethnic variations.

    • Toshihiro Tanaka
    • Yuki Nagata
    • Akira Takemoto
  • The US FDA recently approved mavacamten, a first-in-class myosin modulator, for obstructive hypertrophic cardiomyopathy. By targeting actin mechanobiology, myosin modulators are emerging as important medicines in cardiology.

    • Alfred C. Chin
    • Sharlene M. Day
  • Studies over the past five years showing megakaryocytes in tissues beyond the bone marrow have led scientists to question the definition and purpose of these cells beyond platelet production. Here, we look to evolutionary biology to understand the roles of megakaryocytes in platelet function and diversity and mammalian fitness.

    • Kellie R. Machlus
    • Eric Boilard