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Conlon and Arnold discuss the sex differences in cardiovascular physiology and pathology, the sex chromosome pathways that underlie such differences, and future studies needed to assess how the sex differences are maintained and propagated.
Preserving hemostasis while preventing pathological thrombosis has been a central goal in drug development. A new way to restore hemostasis is suggested by the finding that glycoprotein V is cleaved by thrombin on activated platelets, negatively regulating clotting at sites of vascular injury.
Conlon and Arnold discuss the sex differences in cardiac physiology and pathology, the sex-chromosome pathways underlying such differences, and future studies that are needed to assess how cardiac sex differences are maintained and propagated.
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.
Shakked et al. highlight the importance of cardiomyocytes’ redifferentiation after dedifferentiation and proliferation in cardiac repair and show that redifferentiation depends on negative feedback signaling and LATS1/2 Hippo pathway activity. Cardiomyocyte redifferentiation not only promotes the restoration of cardiac function but also protects against future insult.
Amrute, Lai et al. performed single-nucleus RNA sequencing and compared the cellular and transcriptomic features of hearts from non-diseased donors, from patients with heart failure who recovered systolic function after left ventricular assist device implantation and from patients who did not recover. The analyses identified cell-type-specific signatures of recovery and revealed the downregulation of RUNX1 expression in macrophages and fibroblasts as a predictor of recovery, as confirmed by in silico simulations and re-analysis of data from a mouse model of cardiac functional recovery.