LAUSR

DOI:10.1097/MOL.0000000000000377 Atherosclerosis-related research has focused mainly on the role of endogenous and exogenous lipids (cholesterol, triglycerides, fattyacids, andtheirmodifications) on macrophage foam cell formation, the hallmark feature of early atherogenesis [1 & ,2 & ,3]. Unlike lipids, the contribution of amino acids to the risk of cardiovascular diseases (CVDs) and to atherogenesis was understudied. Recently, a growing body of evidence suggests an important role for some amino acids in the pathogenesis of CVD and atherosclerosis development. Nevertheless, it is important to distinguish between association studies assessing the relationship between plasma levels of such amino acids and CVD risk from mechanistic studies focusing on the biological effects of amino acids on atherogenesis, as these two types of studies often report conflicting findings. The role of the branched chain amino acids (BCAAs; valine, leucine, and isoleucine) in CVD or atherogenesis has been recently studied. Association studies have demonstrated that the plasma levels of BCAAs significantly and independently correlates with dyslipidemia and coronary artery diseases [4]. Despite this association, BCAAs were shown to possess cardio-protectiveeffects inaheart failure ratmodel [5]. Specifically, leucine was reported to attenuate atherosclerosis development in the atherosclerotic apoEdeficent (apoE / ) mice model, by improving the plasma lipid profile and by reducing systemic inflammation [6]. Interestingly, a catabolic defect of BCAAs was identified as a metabolic feature of failing heart, which resulted from Krüppel-like factor 15-mediated transcriptional reprogramming [7 && ]. Therefore, understating the role of BCAA metabolism in the process of macrophage foam cell formation and atherogenesis could be of high importance. Additional amino acids that have been suggested to exert antiatherogenic effects are glycine and arginine.Plasma levelsofglycine, the simplest aminoacid, were found to be inversely associated with the risk of acute myocardial infarction in patients with suspected angina pectoris [8]. A possible mechanism for the antiatherogenic effects of glycine could be related to glycine-gated chloride channels and to glycine-