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Background  Omega‐3 polyunsaturated fatty acids (ω3  PUFA s) suppress inflammation through activation of free fatty acid receptor 4 ( FFAR 4), but this pathway has not been explored in the context of cardiovascular disease. We aimed to elucidate the involvement of  FFAR 4 activation by ω3  PUFA s in the process of vascular inflammation and neointimal hyperplasia in mice.    Methods and Results  We used mice with disruption of  FFAR 4 ( Ffar4  −/− ), along with a strain that synthesizes high levels of ω3  PUFA s ( fat‐1 ) and a group of crossed mice ( Ffar4  −/− / fat‐1 ), to elucidate the role of  FFAR 4 in vascular dysfunction using acute and chronic thrombosis/vascular remodeling models. The presence of  FFAR 4 in vascular‐associated cells including perivascular adipocytes and macrophages, but not platelets, was demonstrated. ω3  PUFA s endogenously generated in  fat‐1  mice (n=9), but not in compound  Ffar4  −/− / fat‐1  mice (n=9), attenuated femoral arterial thrombosis induced by FeCl 3 . Neointimal hyperplasia and vascular inflammation in the common carotid artery were significantly curtailed 4 weeks after FeCl 3  injury in  fat‐1  mice (n=6). This included greater luminal diameter and enhanced blood flow, reduced intima:media ratio, and diminished macrophage infiltration in the vasculature and perivascular adipose tissue compared with control mice. These effects were attenuated in the  Ffar4  −/− / fat‐1  mice.    Conclusions  These results indicate that ω3  PUFA s mitigate vascular inflammation, arterial thrombus formation, and neointimal hyperplasia by interaction with  FFAR 4 in mice. Moreover, the ω3  PUFA – FFAR 4 pathway decreases inflammatory responses with dampened macrophage transmigration and infiltration.

journal of the american heart association

Endogenously Generated Omega‐3 Fatty Acids Attenuate Vascular Inflammation and Neointimal Hyperplasia by Interaction With Free Fatty Acid Receptor 4 in Mice