Abstract
Aging is one major risk factor for the incidence of cardiovascular diseases and the development of atherosclerosis. One important enzyme known to be involved in aging processes is Telomerase Reverse Transcriptase (TERT). After the discovery of the enzyme in humans, TERT had initially only been attributed to germ line cells, stem cells and cancer cells. However, over the last few years it has become clear that TERT is also active in cells of the cardiovascular system including cardiac myocytes, endothelial cells, smooth muscle cells and fibroblasts. Interference with the activity of this enzyme greatly contributes to cardiovascular diseases. This review will summarize the findings on the role of TERT in cardiovascular cells. Moreover, recent findings concerning TERT in different mouse models with respect to cardiovascular diseases will be described. Finally, the extranuclear functions of TERT will be covered within this review.
Highlights
The ends of chromosomes are capped with telomeres, which protect the chromosomes from end-to-end fusion
The Telomerase holoenzyme consists of the catalytic subunit Telomerase Reverse Transcriptase (TERT) and the non-coding Telomerase RNA Component (TERC), which serves as the template for the elongation of the telomere sequences by TERT [1]
This review will focus on the role of Telomerase and in particular of TERT in the heart coronary artery disease and chronic heart failure [28,29] indicating that physical exercise could be in the vessels
Summary
The ends of chromosomes are capped with telomeres, which protect the chromosomes from end-to-end fusion. There is accumulating evidence that substantial Telomerase activity is present in differentiated, non-dividing somatic cells of the cardiovascular system (Figure 1A) [5,6,7,8,9]. This is of particular importance since cardiovascular diseases (CVD) are still the leading cause of death worldwide. TERT expression and Telomerase activity; (B) TERT deficiency completely blunts the protective effects approaches improves cardiac outcome and significantly reduces mortality. Increasing TERT levels in the heart using transgenic or viral
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