Circulating leukocyte telomere length and oxidative stress: a new target for statin therapy

We investigated the relationship between prior statin therapy and leukocyte telomere length (LTL), as well as their interaction with potential new biomarkers of oxidative deoxyribonucleic acid (DNA) lesions and reactive oxygen species-induced inflammation.

From patients admitted for an acute myocardial infarction, LTL was assessed by quantitative polymerase chain reaction (Q-PCR), and leukocyte Finkel-Biskis-Jinkins osteosarcoma (FOS) and 8-oxoguanine DNA glycosylase (OGG1) messenger ribonucleic acid (mRNA) levels were measured by retrotranscription Q-PCR. Patients under prior chronic statin therapy were compared with patients without statin therapy. Although patients on statin therapy were older, their mean LTL was longer than patients not under statin therapy (1.29 ± 0.11 vs. 1.25 ± 0.11 T/S ratio, p = 0.008). In contrast, FOS and OGG1 mRNA levels were similar for the 2 groups. LTL decreased with increasing age, FOS, and OGG1 mRNA levels. Statin therapy remained associated with longer LTL, even after adjustment for confounding factors (p = 0.001), and in younger patients (≤ 64 y). Even in groups matched for propensity scores for statin use, LTL was markedly longer in patients under statin therapy.

Our observational study showed that statin therapy was associated with longer LTL. These data bring to light opportunities to identify new targets for early primary preventive treatment strategies. Moreover, our study raised FOS and OGG1 as new relevant biomarkers of LTL.