Abstract

In this issue of Hypertension , Yang et al1 report that leukocyte telomere length (LTL) is shorter in hypertensive patients than in their normotensive peers. What’s more, after 5 years of follow-up, the authors observed that hypertensive patients with short LTL were more likely to develop atherosclerotic coronary artery disease, whereas normotensive persons with short LTL were more likely to become hypertensive. Several features of this study merit attention. First, the study was conducted in a Chinese cohort, whereas the information we have about the relationships between LTL and cardiovascular risks is primarily derived from white populations. Second, the size of the cohort (388 hypertensive and 379 normotensive persons) and the meticulous attention devoted to characterizing hypertension lend credibility to the findings. Third, the 5-year follow-up period provided the opportunity to explore the potential cardiovascular ramifications of having a short LTL. Thus, the findings of this work indicate that the association between LTL and risks for coronary artery atherosclerosis apply not only to white but also to Chinese populations. What is the biological meaning of the associations between LTL and aging-related diseases, principally atherosclerosis and its risk factors? The short answer is: we do not know. What we do know is that LTL is highly variable at birth and throughout life.2 We also know that age-dependent LTL shortening is much faster in early life than during adulthood,3 probably because of the rapid proliferation of hematopoietic stem cells (HSCs) during growth and development. In fact, LTL shortening throughout life largely mirrors telomere shortening in HSCs. In these cells, like in other somatic cells with rudimentary activity of telomerase (the reverse transcriptase that adds telomere repeats onto …

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