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Showing 1–11 of 11 results
Advanced filters: Author: Zaverio M. Ruggeri Clear advanced filters

  • Blood coagulation protects from microbial infections. A recent study now shows that neutrophils fine tune the procoagulant response to invading pathogens (pages 887–896). Neutrophils degrade an inhibitor of coagulation, locally 'trapping' bacteria in small blood vessels. But they also increase blood clots in large vessels in the absence of infection, which may be relevant for the treatment of thrombosis.

    • Wolfram Ruf
    • Zaverio M Ruggeri
    News & Views
    Nature Medicine
    Volume: 16, P: 851-852

  • Thrombosis complicates SARS-CoV-2 infection and vaccination. Recent data are being used to identify the autoimmune antibody repertoires responsible for the excessive activation of coagulation and platelets.

    • Zaverio M. Ruggeri
    • Wolfram Ruf
    News & Views
    Nature Immunology
    Volume: 22, P: 1352-1353

  • Through genetic mouse models, pharmacological interventions and in vitro assays, Beck et al. show that thrombin-mediated platelet glycoprotein V (GPV) shedding does not affect platelet activation but prevents excessive thrombin-mediated fibrin deposition and thereby controls hemostasis, thrombosis and thrombo-inflammation. The GPV-mediated spatio-temporal control of fibrin formation on thrombogenic surfaces could be targeted to restrict thrombosis while preserving hemostasis.

    • Sarah Beck
    • Patricia Öftering
    • Bernhard Nieswandt
    ResearchOpen Access
    Nature Cardiovascular Research
    Volume: 2, P: 368-382

  • Platelets derive from large precursor cells (megakaryocytes) in the bone marrow. Düttinget al. show that megakaryocyte polarization and platelet biogenesis in the bone-marrow sinusoids are directed by adhesion receptor GPIb signalling and resulting balanced antagonism between RhoA (stop-signal) and Cdc42 (go-signal).

    • Sebastian Dütting
    • Frederique Gaits-Iacovoni
    • Bernhard Nieswandt
    ResearchOpen Access
    Nature Communications
    Volume: 8, P: 1-13

  • Activation of integrin αIIbβ3 at the surface of platelets is required for their aggregation and for thrombus formation. Here Xu et al. identify apolipoprotein A-IV as a novel ligand for platelet αIIbβ3 integrin, and find it inhibits platelet aggregation and thrombosis.

    • Xiaohong Ruby Xu
    • Yiming Wang
    • Heyu Ni
    ResearchOpen Access
    Nature Communications
    Volume: 9, P: 1-18

  • The participation of platelets in atherogenesis and the subsequent formation of occlusive thrombi depend on platelets' adhesive properties and the inability to respond to stimuli with rapid activation. By understanding the multifaceted mechanisms involved in platelet interactions with vascular surfaces and aggregation, new approaches can be tailored to selectively inhibit the pathways most relevant to the pathological aspects of atherothrombosis.

    • Zaverio M. Ruggeri
    Reviews
    Nature Medicine
    Volume: 8, P: 1227-1234