Abstract

Abstract Telomeres are specialized regions of repetitive sequences that found at each end of chromosomes and have an important function in protecting the genomic integrity. In the absence of telomerase functioning in the proliferating cells, every mitotic division progressively shorten telomeres which ultimately leads to senescence of the cells. Therefore, shortening of telomeres’ length is recognized as a mechanism having important functional implications and believed to reflect cellular ageing. However, shortening of telomeres is not the only factor which determines destiny of the cells. Another critical factor affecting this fate is the presence of telomerase which is a polymerase ezyme buffering telomere shortening. Telomere biology has been implicated not only in the cell ageing process, but also in multiple aging-associated conditions and diseases.The critical roles of temomeres and telomerase in cellular ageing and possibly in disease have been demonstrated in recent studies. The experimental findings indicate oxidative stress as a key determinant for telomere shortening which may lead to the hypothesis of telomerase levels may be evaluated as a response to oxidative stress. Oxidative stress is recognized as one of the primary pathogenetic mechanisms involved in COPD, and in particular COPD exacerbation. Our recent finding indicates that the serum levels of telomerase were increased in COPD patients during the attack period.

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