A large variability in occurrence, complications,and age/gender manifestations characterizes individualsusceptibility of sporadic thoracic aortic aneurysms(TAA), even in subjects with the same risk factorprofiles. The reasons are poorly understood. On theother hand, TAA pathophysiology mechanisms remainunclear than those involved in abdominal aorta aneurysms.However, recent evidence is suggesting a crucialrole of biological ageing in inter-individual risk variationof cardiovascular diseases, including sporadicTAA. Biological age rather than chronological age is abetter predictor of vascular risk. Relevant assumptionssupport this concept. In confirming this evidence andour preliminary data, the mean of blood leukocyte telomerelength, through use of terminal restriction fragmentassay and in blood samples from sporadic TAApatients and controls, was examined. Telomerase activitywas also analyzed in two groups. In addition, weverified the weight of genetic inflammatory variants andthe major TAA risk factors in telomere/telomerase impairment.Aorta histopathological abnormalities andsystemic inflammatory mediators were ultimatelycorrelated with telomere/telomerase impairment. Dataobtained demonstrated shorter telomeres and a reducedtelomerase activity in TAA patients significantly associatedwith a genetic inflammatory risk profile, age,gender, smoking, hypertension, a histopathological phenotype,and higher levels of systemic inflammatorymediators than controls. In conclusion, telomere andtelomerase activity’s detection might be used as predictorbiomarkers of sporadic TAA. Their impairment alsosuggests a strong role of vascular ageing in sporadicTAA, evocated by both environmental and genetic inflammatoryfactors.
|Numero di pagine||15|
|Stato di pubblicazione||Published - 2014|
All Science Journal Classification (ASJC) codes