Abstract
Many diseases that involve malignant tumors in the elderly affect the quality of human life; therefore, the relationship between aging and pathogenesis in geriatric diseases must be under-stood to develop appropriate treatments for these diseases. Recent reports have shown that epigenetic regulation caused by changes in the local chromatin structure plays an essential role in aging. This review provides an overview of the roles of telomere shortening on genomic structural changes during an age-dependent shift in gene expression. Telomere shortening is one of the most prominent events that is involved in cellular aging and it affects global gene expression through genome rearrangement. This review provides novel insights into the roles of telomere shortening in disease-affected cells during pathogenesis and suggests novel therapeutic approaches.
Highlights
Telomeres are repetitive sequences that are located at the ends of human chromosomes and are known to constitute ribonucleocomplexes that play a vital role in genome stability
It has been shown that TRF2 (Telomeric repeat binding factor 2) and RAP1 (Repressor/activator protein 1) proteins play central roles in the inhibition of HR (Homology-directed repair) at chromosomal ends, followed by telomere fusion [4,5,6,7]
Since TRF2 and RAP1 are major factors in the human shelterin complex [8], maintaining an appropriate and sufficient telomere length is very important for genome stability
Summary
Telomeres are repetitive sequences that are located at the ends of human chromosomes and are known to constitute ribonucleocomplexes that play a vital role in genome stability. Telomere fusion is closely related to the early development of cancer cells, and it is known to induce aneuploidy in cancer cells through the rearrangement of chromosomes [1,2,3]. It has been shown that TRF2 (Telomeric repeat binding factor 2) and RAP1 (Repressor/activator protein 1) proteins play central roles in the inhibition of HR (Homology-directed repair) at chromosomal ends, followed by telomere fusion [4,5,6,7]. Since TRF2 and RAP1 are major factors in the human shelterin complex [8], maintaining an appropriate and sufficient telomere length is very important for genome stability
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