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Connection between Telomerase Activity in PBMC and Markers of Inflammation and Endothelial Dysfunction in Patients with Metabolic Syndrome

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Autor
Rentoukas, E.; Tsarouhas, K.; Kaplanis, I.; Korou, E.; Nikolaou, M.; Marathonitis, G.; Kokkinou, S.; Haliassos, A.; Mamalaki, A.; Kouretas, D.; Tsitsimpikou, C.
Fecha
2012
DOI
10.1371/journal.pone.0035739
Materia
ASYMMETRIC DIMETHYLARGININE ADMA
BLOOD MONONUCLEAR-CELLS
CORONARY-ARTERY-DISEASE
HEMODIALYSIS-PATIENTS
OXIDATIVE STRESS
NITRIC-OXIDE
ASSOCIATION
ATHEROSCLEROSIS
ACTIVATION
MECHANISMS
Multidisciplinary Sciences
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Resumen
Metabolic syndrome (MS) is a constellation of metabolic derangements associated with vascular endothelial dysfunction and oxidative stress and is widely regarded as an inflammatory condition, accompanied by an increased risk for cardiovascular disease. The present study tried to investigate the implications of telomerase activity with inflammation and impaired endothelial function in patients with metabolic syndrome. Telomerase activity in circulating peripheral blood mononuclear cells (PBMC), TNF-alpha, IL-6 and ADMA were monitored in 39 patients with MS and 20 age and sex-matched healthy volunteers. Telomerase activity in PBMC, TNF-alpha, IL-6 and ADMA were all significantly elevated in patients with MS compared to healthy volunteers. PBMC telomerase was negatively correlated with HDL and positively correlated with ADMA, while no association between TNF-alpha and IL-6 was observed. IL-6 was increasing with increasing systolic pressure both in the patients with MS and in the healthy volunteers, while smoking and diabetes were positively correlated with IL-6 only in the patients' group. In conclusion, in patients with MS characterised by a strong dyslipidemic profile and low diabetes prevalence, significant telomerase activity was detected in circulating PBMC, along with elevated markers of inflammation and endothelial dysfunction. These findings suggest a prolonged activity of inflammatory cells in the studied state of this metabolic disorder that could represent a contributory pathway in the pathogenesis of atherosclerosis.
URI
http://hdl.handle.net/11615/32617
Colecciones
  • Δημοσιεύσεις σε περιοδικά, συνέδρια, κεφάλαια βιβλίων κλπ. [19735]
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