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首页> 外文OA文献 >Are the leukocyte telomere length attrition and telomeraseudactivity alteration potential predictor biomarkers for sporadicudTAA in aged individuals?
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Are the leukocyte telomere length attrition and telomeraseudactivity alteration potential predictor biomarkers for sporadicudTAA in aged individuals?

机译：是白细胞端粒长度减员和端粒酶 ud散发性/ ud的活动改变潜能预测生物标志物老年人中的TAA？

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A large variability in occurrence, complications,udand age/gender manifestations characterizes individualudsusceptibility of sporadic thoracic aortic aneurysmsud(TAA), even in subjects with the same risk factorudprofiles. The reasons are poorly understood. On theudother hand, TAA pathophysiology mechanisms remainudunclear than those involved in abdominal aorta aneurysms.udHowever, recent evidence is suggesting a crucialudrole of biological ageing in inter-individual risk variationudof cardiovascular diseases, including sporadicudTAA. Biological age rather than chronological age is audbetter predictor of vascular risk. Relevant assumptionsudsupport this concept. In confirming this evidence andudour preliminary data, the mean of blood leukocyte telomereudlength, through use of terminal restriction fragmentudassay and in blood samples from sporadic TAAudpatients and controls, was examined. Telomerase activityudwas also analyzed in two groups. In addition, weudverified the weight of genetic inflammatory variants andudthe major TAA risk factors in telomere/telomerase impairment.udAorta histopathological abnormalities andudsystemic inflammatory mediators were ultimatelyudcorrelated with telomere/telomerase impairment. Dataudobtained demonstrated shorter telomeres and a reducedudtelomerase activity in TAA patients significantly associatedudwith a genetic inflammatory risk profile, age,udgender, smoking, hypertension, a histopathological phenotype,udand higher levels of systemic inflammatoryudmediators than controls. In conclusion, telomere andudtelomerase activity’s detection might be used as predictorudbiomarkers of sporadic TAA. Their impairment alsoudsuggests a strong role of vascular ageing in sporadicudTAA, evocated by both environmental and genetic inflammatoryudfactors.
机译：即使在具有相同危险因素 udprofile的受试者中，散发性胸主动脉瘤 ud（TAA）的发生，并发症，年龄和性别表现的差异也很大。原因尚不清楚。另一方面，TAA的病理生理机制仍然比涉及腹主动脉瘤的机制还不清楚。 ud然而，最近的证据表明，生物衰老在个体间风险变异，心血管疾病（包括偶发性 udTAA）中起着至关重要的作用。生物年龄而非年龄是血管风险的更好预测指标。相关假设 ud支持此概念。为了证实这一证据和的初步数据，检查了通过使用末端限制性酶切片段片段法/散剂和散发的TAA 患者和对照组的血液样本中白细胞端粒的平均长度超长。还对两组的端粒酶活性进行了分析。此外，我们研究了端粒/端粒酶损伤中遗传炎症变种的权重和主要的TAA危险因素。 udAorta的组织病理学异常和系统性炎症介质最终与端粒/端粒酶损伤不相关。数据 u003b u003b u003b u003b u003b u003b u003b u003b u003b u003b u003b u003b u003b u003b u003b u003b u003b u003b u003b 结果的结果表明，TAA患者的端粒较短，端粒酶活性降低与遗传性炎症风险特征，年龄，性别，吸烟，高血压，组织病理学表型和全身炎性介质的水平明显高于对照组。总之，端粒和 udomeromerase活性的检测可以用作散发TAA的预测指标 udbiomarker。它们的损害也提示血管衰老在散发的udTAA中起着重要作用，这是由环境和遗传性炎症因素引起的。

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