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Editorial
. 2018 Feb;6(3):56.
doi: 10.21037/atm.2017.11.36.

Protease activated receptor 4: a backup receptor or a dark horse as a target in antiplatelet therapy?

Affiliations
Editorial

Protease activated receptor 4: a backup receptor or a dark horse as a target in antiplatelet therapy?

Xu Han et al. Ann Transl Med. 2018 Feb.
No abstract available

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Conflict of interest statement

Conflicts of Interest: The authors have no conflicts of interest to declare.

Figures

Figure 1
Figure 1
Platelet activation and current anti-platelet therapeutic strategies. (A) Schematic demonstration of the major signaling pathways involved in platelet adhesion and activation. The primary receptors on the surface of the platelet, GPCRs (PARs, P2Ys, and TP), GPVI and the GPIb-XI-V complex are essential for activating second messengers that lead to shape change and granule secretion; (B) the drugs and experimental compounds that have been developed targeting the key receptors on the surface of platelets are shown. GPCR, G-protein coupled receptor; PAR, protease activated receptor; TP, thromboxane receptor; GPVI, Glycoprotein VI.
Figure 2
Figure 2
Comparison of PAR1 and PAR4 signaling in platelets and the chemical structures of four PAR4 antagonists. (A) PAR1 and PAR4 have overlapping and unique roles in platelet activation. These two GPCRs couple to the same G-proteins, however with distinct kinetics, which has important physiological consequence; (B) chemical structures of the four compounds that have PAR4 antagonism effect. PAR, protease activated receptor; GPCR, G-protein coupled receptor.

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References

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