N1‐methylnicotinamide (MNAM) as a guardian of cardiovascular system. Issue 10 (9th May 2018)

• Record Type: Journal Article
• Authors: Nejabati, Hamid Reza; Mihanfar, Aynaz; Pezeshkian, Masoud; Fattahi, Amir; latifi, Zeinab; Safaie, Naser; Valiloo, Mohammad; Jodati, Ahmad Reza; Nouri, Mohammad
• Is Part Of: Journal of cellular physiology. Volume 233:Issue 10(2018:Oct.)
• Page Start: 6386
• Page End: 6394
• Publication Date: 2018-05-09
• Subjects: atherosclerosis -- coronary artery disease -- lipid droplets -- N‐methyltransferase -- N1‐methylnicotinamide; Physiology -- Periodicals; Cell physiology -- Periodicals; 571.6
• DOI: 10.1002/jcp.26636
• Languages: English
• ISSNs: 0021-9541

Abstract

Abstract : Atherosclerosis is identified as the formation of atherosclerotic plaques, which could initiate the formation of a blood clot in which its growth to coronary artery can lead to a heart attack. N‐methyltransferase (NNMT) is an enzyme that converts the NAM (nicotinamide) to its methylated form, N1‐methylnicotinamide (MNAM). Higher levels of MNAM have been reported in cases with coronary artery disease (CAD). Further, MNAM increases endothelial prostacyclin (PGI2) and nitric oxide (NO) and thereby causes vasorelaxation. The vasoprotective, anti‐inflammatory and anti‐thrombotic roles of MNAM have been well documented; however, the exact underlying mechanisms remain to be clarified. Due to potential role of MNAM in the formation of lipid droplets (LDs), it might exert its function in coordination with lipids, and their targets. In this study, we summarized the roles of MNAM in cardiovascular system and highlighted its possible mode of actions. Abstract : In inflammatory conditions like atherosclerosis, elevated levels of inflammatory cytokines such as TNFα induce NNMT expression and so that increase circulating MNAM which improves endothelial functions via facilitating PUFAs uptake, the formation of unsaturated LDs, and increasing the PGI2, and NO release.