Abstract

Telomere (TL) is a biomarker of biological aging, and its shortening is associated with major risk factors for cardiovascular diseases (CVD). This study aimed to identify whether TL is associated with arterial stiffness as reflected by brachial–ankle pulse wave velocity (baPWV). This population-based cross-sectional study involved 1065 individuals in the Iwaki area, Japan. Total TL length and TL G-tail length were measured by hybridization protection assay. The baPWV was measured on the right and left sides using a non-invasive vascular screening device. The associations between TL and baPWV were assessed by multivariate linear regression. Compared with the shortest total TL tertile, the longest total TL group showed a significant decrease in baPWV (lowest vs. highest tertile: adjusted beta: −41.24, 95% confidence interval (CI): −76.81, −5.68). The mean baPWV decreased with a longer TL (TL G-tail length: p trend < 0.001, total TL: p trend < 0.001). TL G-tail and total TL lengths were inversely associated with baPWV, implicating TL shortening in the development of CVD. This study provides evidence of the factors influencing CVD risks at a very early stage when individuals can still take necessary precautions before CVD gives rise to a symptomatic health outcome.

Highlights

  • Telomeres (TLs) are repeated sequences of TTAGGG oligomer caps at the chromosomal ends [1,2]

  • The mean brachial–ankle pulse wave velocity (baPWV) of the study analyzed the data of 1056 participants

  • Considering that TL is associated with arterial stiffness across the life course, our findings offer an important insight into TL as an underlying factor for the development of cardiovascular diseases (CVD)

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Summary

Introduction

Telomeres (TLs) are repeated sequences of TTAGGG oligomer caps at the chromosomal ends [1,2]. TLs are involved in maintaining cellular integrity by protecting end-to-end chromosomal fusion [1,3]. TLs shorten with each cell division, and subsequent cellular senescence occurs when they reach a critical length [1]. DNA polymerase fails to fully replicate at the terminal 3 -end of DNA, resulting in the extension of G-rich repeats known as the TL G-tail [4]. The G-tail plays a critical role in the formation of the T-loop, essential for hiding the terminal end of TLs and preventing end-to-end fusion [2,5]. In addition to total TL length, telomere G-tail length acts as a marker of biological aging

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