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In endothelial cells, inflammatory cytokines such as interferons, tumour necrosis factor alpha or interleukins increase oxidative stress and contractile prostanoids and the expression of adhesion molecules that reduce nitric oxide (NO) availability and bind leucocytes, thereby impairing endothelial function. Despite this evidence, anti\u2010inflammatory therapies are not yet indicated for the treatment of most CVD. Resolution of inflammation is mediated by a family of specialized pro\u2010resolving mediators (SPMs) that act on cognate G protein\u2013coupled receptors to limit immune cell infiltration and initiate tissue repair. SPMs, generated from omega\u20103 and omega\u20106 polyunsaturated fatty acids, belong to four major families: lipoxins, resolvins, protectins and maresins. SPM receptors are expressed in immune and vascular cells where they regulate important processes such as phagocytosis and polarization, production of cytokines, NO and prostacyclin, and modulation of smooth muscle cell phenotype. Growing evidence in animal models demonstrates that activation of SPM receptors can protect vascular function and structure and provide beneficial effects in various CVD. 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