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Telomere/telomerase system impairment in circulating angiogenic cells of geriatric patients with heart failure

F Olivieri1, R Antonicelli, R Recchioni

  • 1Department of Molecular Pathology and Innovative Therapies, Università Politecnica delle Marche, Ancona, Italy. f.olivieri@univpm.it

International Journal of Cardiology
|July 9, 2011
PubMed

Insights

Circulating angiogenic cells (CACs) in heart failure patients show impaired telomere length and telomerase activity. This telomere/telomerase system dysfunction in CACs offers new insights into congestive heart failure (CHF) pathogenesis.

Area of Science:

  • Cardiovascular Research
  • Cell Biology
  • Aging Research

Background:

  • Circulating angiogenic cells (CACs) functional capacity is compromised in congestive heart failure (CHF) patients.
  • The precise mechanisms underlying CAC dysfunction in CHF remain incompletely understood.
  • No prior studies have investigated the telomere/telomerase system in CACs from CHF patients.

Purpose of the Study:

  • To investigate telomere length and telomerase activity in CACs of CHF patients.
  • To compare these parameters between CHF patients and healthy controls.
  • To explore the association of telomere/telomerase system with CHF markers.

Main Methods:

  • Collected CACs and leukocytes from 40 CHF patients and 40 healthy controls.
  • Assessed telomere length (T/S ratio) and telomerase (TERT) activity in CACs and leukocytes.
  • Utilized Receiver Operator Characteristic (ROC) analysis to evaluate diagnostic accuracy.
  • Measured CD34+/VEGFR2+ cell counts and plasma levels of IL-6 and TNF-α.

Main Results:

  • CHF patients exhibited significantly reduced CAC telomere length (T/S ratio) and telomerase activity compared to controls.
  • Leukocytes showed a significant reduction in T/S ratio but not telomerase activity.
  • CAC T/S ratio demonstrated higher diagnostic accuracy (AUC=0.89) for CHF than leukocyte T/S ratio (AUC=0.73).
  • Increased CD34+/VEGFR2+ cells and elevated IL-6/TNF-α levels were observed in CHF patients.

Conclusions:

  • CACs in CHF patients display significant impairment in their telomere/telomerase system.
  • This telomere/telomerase dysfunction in CACs contributes to the understanding of CHF pathogenesis.
  • Telomere/telomerase system assessment in CACs may hold clinical relevance for CHF patients.
Abstract

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