Key result
Ionizing radiation exposure is hypothesized to cause detrimental vascular effects through the crucial mediator of telomere shortening.
This review proposes the hypothesis that telomere shortening may be a crucial mediator of vascular dysfunction and atherosclerotic disease following exposure to ionizing radiation.
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May link radiation to vasculopathy via telomeres; leaves open mechanistic confirmation and interventional trials.
PURPOSE: In recent years, growing epidemiological evidence has linked ionizing radiation exposure to cardiovascular atherosclerotic disease. However, there are still major gaps in the knowledge of the molecular mechanisms of radiation-induced vascular disease, especially for low-dose levels. Telomeres, repetitive DNA sequences of (TTAGGG)(n) located at the ends of eukaryotic chromosomes, play a role in regulating vascular aging, and shorter leukocyte telomere length has been demonstrated to predict cardiovascular disease and mortality. There is also evidence supporting the crucial role of telomeres in the formation of chromosome and chromatid aberrations induced by ionizing radiation. CONCLUSIONS: The purpose of the present paper is to review the recent advances in the biological mechanisms determining telomere length erosion after ionizing radiation exposure as well as to examine the hypothesis that telomere shortening may be the crucial mediator leading to detrimental vascular effects after ionizing radiation exposure.
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Sabatino et al. (2012) conducted a review in Cardiovascular atherosclerotic disease. Ionizing radiation exposure was evaluated. Ionizing radiation exposure is hypothesized to cause detrimental vascular effects through the crucial mediator of telomere shortening.
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