MaR1 receptors are still unknown, however a recent report showed partial inhibition of the effects of MaR1 in dorsal root ganglion neurons, in the presence of pertussis toxin, suggestive of a BMN673 1207456-01-6 decrease in cAMP mediating MaR1’s effects in neurons. In this study, we report MaR1 to elevate intracellular cAMP levels in naive smooth muscle and endothelial cells. A recent study also showed time-dependent elevation of cAMP and PKA activity by resolvin-D1 in mouse RAW 264.7 macrophages. Moreover, we found that MaR1 led to increased cAMP levels in TNF-a treated cells. Cyclic-AMP has been shown to impart anti-inflammatory actions on cytokine activated human endothelial cells and vascular smooth muscle cells, by blocking NF-kB activation and reducing adhesion molecule expression, and therefore forms an important line of investigation related to MaR1’s anti-inflammatory actions on vascular cells. Increased levels of 14-HpDHA have been found in subcutaneous fat surrounding foot wounds in patients with peripheral vascular disease, suggesting activation of resolution pathways involving MaR1 in PVD. In another study, bacterial lipopolysaccharide was found to enhance the synthesis of 14-HpDHA and MaR1 in human Caco-2 epithelial cells and foam macrophages. These observations highlight the importance of MaR1 in activating “anti-inflammatory” and “resolution” signaling pathways in the inflammatory zone or region and underscores its importance in turning “ON” proresolution pathways in these inflammatory diseases. In summary, in the present study we report MaR1 to impart a strong antiinflammatory phenotype in human vascular smooth muscle cells and endothelial cells, associated with reduced monocyte adhesion and TNF-a induced production of ROS and inflammatory mediators. At the molecular level, we found MaR1 to reduce NOX expression and inhibit NF-kB activation and increase intracellular cAMP levels in both cell types. Hence, we conclude that MaR1 has potent anti-inflammatory actions in vascular cells of human origin and modulates signaling pathways under basal and TNFa-stimulated conditions. These findings suggest a therapeutic potential for maresins and their emergence as a novel family of DHA-derived SPMs to treat vascular inflammatory diseases. Calcium channel blockers disrupting the movement of calcium through calcium channels, include dihydropyridine, phenylalkylamine and benzothiazepine. Three kinds of reagents display different molecular structures and bind separately with receptor sites located in or near the calcium channel. Among them, nifedipine is commonly used in the treatment of angina and hypertension. Several epigenetic studies have implicated that CCBs might be involved in cancer stimulation, but the risk of CCBs is controversial. CCBs facilitated the division of cells with malignant potential, thus they increased the risk of cancers especially the breast cancer. In a prospective cohort study, 451 out of 5052 people aged about 71 years had taken CCBs for four years and the hazard ratio for cancer associated with CCBs compared with not taking CCBs was 1.72. Fitzpatrick and colleagues chose 3198 women aged over 65 years from 4 different places.