A pilot study published in a research letter in this week’s issue of THE LANCET suggests that chromosomal changes associated with premature ageing may predispose individuals to atherosclerosis.
Chromosomes end with telomeres, which shorten with cellular ageing; therefore, telomere length can be viewed as a biomarker of cell ageing. Nilesh Samani and colleagues from Leicester University, UK, investigated whether atherosclerosis is associated with systemic evidence of accelerated cellular ageing. The investigators compared the average length of terminal restriction fragments (TRF), a measure of average telomere length, in DNA of circulating white blood cells of ten patients with severe coronary artery disease (CAD) with 20 individuals without CAD (the control group). Adjusting for age and sex, individuals with CAD had average TRF lengths of 303 base pairs shorter compared with the control group; since telomeres of white blood cells shorten on average by about 35 base pairs per year, this reduction among individuals with CAD meant that their cells looked like those of individuals with no CAD who were 8.6 years older.
Nilesh Samani comments: “It was very surprising to find that patients with CAD showed this sign of accelerated cellular ageing in a circulating cell removed from the site of the problem in the coronary artery. It is possible that this simply reflects the effects of other risk factors for CAD such as high blood pressure, diabetes, and cholesterol. On the other hand, it is conceivable that some people are either born with shorter telomeres, or have accelerated telomere-shortening in early life. Since telomere shortening affects cellular function, this, at least partly, is what predisposes these individuals to developing CAD. This is an intriguing possibility with considerable implications for our understanding of the mechanisms leading to this important clinical problem.” (Quote by e-mail; does not appear in published paper).
Journal
The Lancet