Toupance Simon, Labat Carlos, Temmar Mohamed, Rossignol Patrick, Kimura Masayuki, Aviv Abraham, Benetos Athanase
From the INSERM UMRS 1116 (S.T., C.L., P.R., A.B.), Department of Geriatric Medicine, CHRU de Nancy (C.L., A.B.), and Inserm, Centre d'Investigations Cliniques-Plurithématique 14-33, CHRU Nancy (P.R.), Université de Lorraine, Nancy, France; Cardiology Center, Ghardaia, Algeria (M.T.); and Center of Human Development and Aging, Rutgers, The State University of New Jersey, New Jersey Medical School, Newark (M.K., A.A.).
Hypertension. 2017 Aug;70(2):420-425. doi: 10.1161/HYPERTENSIONAHA.117.09354. Epub 2017 Jun 19.
Short telomeres are associated with atherosclerosis. However, the temporal relationship between atherosclerosis and telomere length is unclear. The objective of this work was to examine the temporal formation and progression of carotid atherosclerotic plaques in relation to telomere dynamics. In a longitudinal study, comprising 154 French men and women (aged 31-76 years at baseline), carotid plaques were quantified by echography, and telomere length on leucocytes was measured by Southern blots at baseline and follow-up examinations. Telomere attrition rates during the 9.5-year follow-up period were not different in individuals with plaques at both baseline and follow-up examinations (23.3±2.0 base pairs/y) than in individuals who developed plaques during the follow-up period (26.5±2.0 base pairs/y) and those without plaques at either baseline or follow-up examination (22.5±2.3 base pairs/y; =0.79). At baseline, telomere length was associated with presence of carotid plaques (=0.02) and with the number of regions with plaques (=0.005). An interaction (=0.03) between age and the presence of plaques was observed, such that the association between plaques and telomere length was more pronounced at a younger age. In conclusion, carotid atherosclerosis is not associated with increased telomere attrition during a 9.5-year follow-up period. Short telomere length is more strongly associated with early-onset than late-onset carotid atherosclerosis. Our results support the thesis that heightened telomere attrition during adult life might not explain the short telomeres observed in subjects with atherosclerotic disease. Rather, short telomeres antecedes the clinical manifestation of the disease.
端粒缩短与动脉粥样硬化相关。然而,动脉粥样硬化与端粒长度之间的时间关系尚不清楚。本研究的目的是探讨与端粒动态变化相关的颈动脉粥样硬化斑块的时间形成和进展情况。在一项纵向研究中,纳入了154名法国男性和女性(基线年龄31 - 76岁),通过超声心动图对颈动脉斑块进行定量分析,并在基线和随访检查时通过Southern印迹法测量白细胞端粒长度。在基线和随访检查时均有斑块的个体(23.3±2.0碱基对/年)、随访期间出现斑块的个体(26.5±2.0碱基对/年)以及基线或随访检查时均无斑块的个体(22.5±2.3碱基对/年;P = 0.79)在9.5年随访期内的端粒损耗率无差异。在基线时,端粒长度与颈动脉斑块的存在(P = 0.02)以及斑块区域数量(P = 0.005)相关。观察到年龄与斑块存在之间存在交互作用(P = 0.03),使得斑块与端粒长度之间的关联在较年轻年龄时更为明显。总之,在9.5年的随访期内,颈动脉粥样硬化与端粒损耗增加无关。端粒长度缩短与早发性而非晚发性颈动脉粥样硬化的关联更为密切。我们的结果支持这样的观点,即成年期端粒损耗加剧可能无法解释在动脉粥样硬化疾病患者中观察到的端粒缩短现象。相反,短端粒先于疾病的临床表现出现。