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Editorial
. 2022 Oct 24;7(10):998-1000.
doi: 10.1016/j.jacbts.2022.06.016. eCollection 2022 Oct.

Plasminogen Activator Inhibitor-1: Another String in the Platelet-Derived Extracellular Vesicles Bow?

Dimitri Arangalage  1   2 , Gregory Franck  2 , Giuseppina Caligiuri  1   2
Affiliations
Editorial

Plasminogen Activator Inhibitor-1: Another String in the Platelet-Derived Extracellular Vesicles Bow?

Dimitri Arangalage et al. JACC Basic Transl Sci. .
No abstract available

Keywords: biomarkers; coronary artery disease; extracellular vesicles; plasminogen activator inhibitor-1.

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Conflict of interest statement

The authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Figures

None
Graphical abstract
Figure 1
Figure 1
The Potential Role of PAI-1+ PEV in Coronary Artery Disease Platelet-derived extracellular vesicles expressing plasminogen activator inhibitor-1 (PAI-1+ PEV) promote smooth muscle cell (SMC) phenotypic switching toward a proinflammatory and procalcifying phenotype via the activation of the lipoprotein receptor–related protein 1 (LRP1) receptor. High PAI-1+ PEV levels were predictive of major adverse cardiovascular events (MACE). Inhibition of the PAI-1/LRP1 pathway with TM5275 dampened SMC phenotypic switching. Neither PAI-1+ PEV levels nor TM5275 affected thrombogenicity, but the exact mechanisms remain to be deciphered. VSMC = vascular smooth muscle cell.
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Comment on

  • doi: 10.1016/j.jacbts.2022.05.002

References

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