Table 1.

Potential mechanisms of antiplatelet effects of EPA and DHA.

Number in Figure 2	Haemostasis Component	Potential Mechanism	Effect	Strength of Evidence	Reference
1	Prothrombinase complex (factors Va, Xa, II) on the surface of blood platelets	Decrease in cell membrane fluidity resulting in poor availability of procoagulant phospholipids (phosphatidylserine)	Slower conversion of prothrombin into thrombin; inhibition of coagulation cascade and platelet aggregation	Low	Larson [26]
1a	Ionotropic calcium channels in plasma membrane	Decrease in cell membrane fluidity resulting in reduced influx of Ca2+	Inhibition of blood platelets activation	Low	Kacik [31]
2	Synthesis of TxA2	Competition between AA and EPA for enzymes essential for further metabolic steps	Inhibition of TxA2 synthesis leading to a production of TxA3 having weak pro-aggregatory properties; inhibition of TXA2-dependent platelet activation	High	DeFilippis Adili, Bäck [28,32,33]
2a	Synthesis of TxA2	Metabolite of EPA–resolvin binding to TxA2 receptor	Inhibition of TXA2-dependent platelet activation	Moderate	Sheikh, Bäck [33,34]
3	Receptor for ADP and receptor for thrombin	Metabolite of EPA–resolvin binding to receptors for ADP and thrombin	Inhibition of TXA2-and thrombin-dependent platelet activation	Moderate	Fredman, Dona [30,35]
4	Receptor GPVI (collagen receptor)	Blocking of the receptor (detailed mechanism unknown) or inhibition of platelet reactivity in a glycoprotein VI-dependent manner via activation of protein kinase A	Inhibition of collagen-dependent platelet activation	Low	Larson [36] Yamaguchi [8]