Resialylation of sialic acid deficit vascular endothelium, circulating cells and macromolecules may counteract the development of atherosclerosis: a hypothesis.
Deficit sialylation of vascular endothelium, circulating cells and macromolecules has been associated with the development of atherosclerosis. On the other hand, an elevated serum level of sialic acid is a long-lasting marker of atherosclerosis and complications from atherosclerosis. One may speculate that the inverse associations with atherosclerosis risk are due to some common underlying cause. One mission for the elevated serum sialic acid level might be to act as a substrate for resialylation of sialic acid deficit structures and thereby counteract the atherosclerotic process.
Lindberg
Gunnar
G
The NEPI Foundation (The Swedish Network for Pharmacoepidemiology), Clinical Research Centre, Malmö University Hospital, Malmö, Sweden. gunnar.lindberg@nepi.net <gunnar.lindberg@nepi.net>
D050197:Atherosclerosis / Q000209:etiology / Q000517:prevention & control*; D001792:Blood Platelets / Q000378:metabolism; D004730:Endothelium, Vascular / Q000378:metabolism*; D006017:Glycolipids / Q000378:metabolism; D006023:Glycoproteins / Q000378:metabolism; D006801:Humans; D008264:Macrophages / Q000378:metabolism; D008955:Models, Cardiovascular; D019158:N-Acetylneuraminic Acid / Q000097:blood / Q000378:metabolism*
D006017:Glycolipids; D006023:Glycoproteins; D019158:N-Acetylneuraminic Acid