Review Article
Homocysteine as a Risk Factor for Atherosclerosis: Is Its Conversion to S-Adenosyl-L-Homocysteine the Key to Deregulated Lipid Metabolism?
Table 1
Experimental evidence on deregulation of lipid metabolism and UPR induction under elevated homocysteine levels in yeast and mammals*.
| Experimental evidence | Yeast | Mammals |
| AdoHcy is formed in vivo in response to elevated Hcy levels | + | + |
| AdoHcy is more toxic than Hcy to cells deficient in Hcy catabolism | + | |
| AdoHcy represents a better marker of cardiovascular risk than Hcy | | + |
| Phospholipid methylation is quantitatively the major consumer of AdoMet | + | + |
| Phospholipid methylation is inhibited in response to Hcy supplementation | + | |
| Phospholipid methylation is inhibited by AdoHcy | + | + |
| TAG is accumulating in response to Hcy supplementation | + | + |
| TAG is accumulating in response to deficiency in AdoHcy hydrolysis | + | |
| TAG is accumulating in response to deficiency in phospholipid methylation | + | + |
| UPR is inducted in response to Hcy supplementation | + | + |
| The de novo phospholipid methylation pathway produces phospholipids enriched in unsaturated fatty acids | + | + |
| ER stress is inducted by accumulation of saturated fatty acids in membrane phospholipids | + | + |
| Hcy/AdoHcy levels are inversely correlated to the levels of unsaturated fatty acids | | + |
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*The absence of a plus sign in some columns implies lack of data or nonapplicability.
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