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Figure 1 | Lipids in Health and Disease

Figure 1

From: The “Mevalonate hypothesis”: a cholesterol-independent alternative for the etiology of atherosclerosis

Figure 1

The mevalonate hypothesis. Inflammatory factors like homocysteine can activate the mevalonate pathway. Also reduced uptake of LDL cholesterol (LDL) by LDL receptors (LDL-REC) can activate the mevalonate pathway. The mevalonate pathway regulates numerous biological activities including the formation of coenzyme Q10, the formation of cholesterol and the activation of NADPH oxidase. Activation of NADPH oxidase can contribute to the formation of ox-LDL cholesterol which is probably an important trigger for the induction of atherosclerosis. Coenzyme Q10 plays an important role as an anti-oxidant in the protection of LDL cholesterol from oxidation.

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