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00925njm 22002777a 4500 dc De Meyer, Tim author Nawrot, Tim author Bekaert, Sofie author De Buyzere, Marc L author Rietzschel, Ernst R author Andres, Vicente author 2018-08 Telomeres shorten with age, the major risk factor for atherosclerotic cardiovascular disease (aCVD). The observation of shorter telomeres in aCVD patients thus suggested that critical telomere shortening may contribute to premature biological aging and aCVD. Therefore, telomere length often is suggested as a causal aCVD risk factor, a proposal supported by recent Mendelian randomization studies; however, epidemiological research has shown disappointingly low effect sizes. It therefore remains uncertain whether telomere shortening is a cause of aCVD or merely a consequence. The authors argue that elucidating the mechanistic foundation of these findings is essential for any possible translation of telomere biology to the clinic. Here, they critically evaluate evidence for causality in animal models and human studies, and review popular hypotheses and discuss their clinical implications. The authors identify 4 key questions that any successful mechanistic theory should address, and they discuss how atherosclerosis-associated local telomere attrition may provide the answers. J Am Coll Cardiol. 2018; 72(7):805-813 10.1016/j.jacc.2018.06.014 1558-3597 0735-1097 Journal of the American College of Cardiology 30092957 http://hdl.handle.net/20.500.12105/9670 atherosclerosis biological aging epidemiology telomerase Telomere Length as Cardiovascular Aging Biomarker: JACC Review Topic of the Week