Abstract
Epidemiologic studies in North America and Europe have shown that people consuming Western-type diets are low in magnesium (Mg) content (i.e., < 30 - 65% of the RDA for Mg); most such diets in the USA show that 60 - 80% of Americans are consuming only 185 - 235 mg/day of Mg. Low Mg content in areas of soft-water, and Mg-poor soil, is associated with high incidences of ischemic heart disease (IHD), coronary artery disease, hypertension, and sudden cardiac death (SCD). It is clear that the leading underlying cause of death worldwide is atherosclerosis. Importantly, both animal and human studies have shown an inverse relationship between dietary intake of Mg and atherosclerosis. The myocardial level of Mg has consistently been observed to be lower in subjects dying from IHD and SCD in soft-water areas than those in hard-water areas. Over the past 20 years, our laboratories, using several types of primary cultured vascular smooth muscle (VSM) cells, and myocardial cells, demonstrated that declining levels of extracellular Mg ([Mg2+]0) activated several enzymatic pathways to produce increases in cellular sphingolipids, particularly ceramides which are known to exert numerous types of cardiovascular manifestations including inflammatory effects ; the latter play important roles in atherogenesis and cardiovascular diseases. Approximately 20 years ago, we reported that low [Mg2+]0 caused formation of platelet-activating factor (PAF) as well as other types of PAF-like molecules and suggested that these molecules might be causative agents in low Mg2+- induced IHD and SCD. Herein, we review results and data from our labs which strongly support roles for ceramides, PAF and PAF-like lipids in low [Mg2+]0-induced IHD and SCD.
Highlights
Several epidemiologic studies in North America and Europe have shown that people consuming Western-type diets are low in magnesium (Mg) content
We have demonstrated that feeding the animals diets low in Mg results in all of the hallmarks of atherosclerosis, i.e., inflammation followed by release of hydrolytic enzymes, release of cytokines, release of chemokines and growth factors involved in the early stages of the atherogenic process demonstrating lesions and plaques on the inner surfaces of the endothelial walls followed by invasion of vascular smooth muscle (VSM) cells which become transformed phenotypes [4,16,17,43,45]
What are the cellular and molecular events leading to inflammatory events, release of hydrolytic enzymes, release of cytokines, chemokine’s and growth factors, and transformation of contractile VSM cells to non-contractile VSM cells which behave as machines to synthesize and release these pro-atherogenic molecules? It has been shown by our group [4,25,43,51] and others [52,53,54] that ceramides, in increased levels, found in the atherogenic process[mixed in plaques; unpublished findings ], at least in rabbits, and stimulated in MgD states could be important causal and initiating agents [16,17]
Summary
Open Access: Potential Roles of Magnesium Deficiency in Inflammation and Atherogenesis: Importance and Cross-talk of Platelet-Activating Factor and Ceramide. Altura BM1,2,3,4,5*, Gebrewold A1, Shah NC1,5, Shah GJ1,5 and Altura BT1,3,4,5 1Department of Physiology and Pharmacology, State University of New York Downstate Medical Center, Brooklyn, New York, USA 2Department of Medicine, State University of New York Downstate Medical Center, Brooklyn, New York, USA 3Center for Cardiovascular and Muscle Research, State University of New York Downstate Medical Center, Brooklyn, New York, USA 4The School of Graduate Studies in Molecular and Cellular Science, State University of New York Downstate Medical Center, Brooklyn, New York, USA 5Bio-Defense Systems, Inc, Rockville Centre, New York, USA
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