Transthyretin protein may accelerate atherosclerosis

Scientists report in the November 2007 issue of the Journal of Lipid Research that a protein called transthyretin (TTR) that is present in the blood may accelerate the development of atherosclerosis - a potentially fatal heart disease in which the arteries are progressively narrowed and hardened over time, reducing blood flow to the heart.

TTR has been shown to cleave a blood compound called apolipoprotein A-I (ApoA-I), which can produce structures called fibrils that are shaped like strands and accumulate in blood vessels. These fibrils have been observed in people with a mutation of the gene that makes ApoA-I, but whether cleavage by TTR promotes the formation of such fibrils has not been assessed yet.

Monica Mendes Sousa and colleagues determined that when ApoA-I is cleaved by TTR, it tends to form fibrils faster than the uncleaved ApoA-I. This discovery may provide new ways to treat people with atherosclerosis by stopping TTR from cleaving ApoA-I and slowing down the formation of fibrils in blood vessels

Article: “ApoA-I cleaved by transthyretin has reduced ability to promote cholesterol efflux and increased amyloidogenicity,” by Marcia Almeida Liz, Claudio M. Gomes, Maria Joao Saraiva, and Monica Mendes Sousa

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