Homocysteine Upregulates 3-Hydroxy-3-Methylglutaryl Coenzyme A Reductase in Vascular Endothelial Cells

The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 6 No. 1 • February 2003


Homocysteine Upregulates 3-Hydroxy-3-Methylglutaryl Coenzyme A Reductase in Vascular Endothelial Cells

The statins are a relatively new class of drugs that are effective in the reduction of cholesterol by inhibiting the rate-limiting enzyme in the synthesis of cholesterol, 3-hydroxy-3-methylglutaryl coenzyme A reductase. Statins also have a number of other effects, including increasing endothelial nitric oxide release.

A new study1 found, by screening human umbilical-vein endothelial cells with complementary DNA microarray for the gene expression modified by homocysteine, that 3-hydroxy-3-methylglutary1 coenzyme A reductase is increased by homocysteine. This, then, appears to be yet another mechanism by which homocysteine increases the risk of cardiovascular disease, in this case by increasing the production of cholesterol.

Moreover, some statins have been found to reduce cardiovascular disease risks more than expected by their effects on cholesterol alone. Perhaps their interference with homocysteine signaling has something to do with this.

Reference

  1. Li et al. Homocysteine induces 3-hydroxy-3-methylglutaryl coenzyme A reductase in vascular endothelial cells. Circulation 105:1037-43 (2002).

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