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-American Society for Biochemistry and Molecular Biology