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Telomere maintenance refers to the process by which cells preserve the length and integrity of telomeres—repetitive DNA–protein structures at the ends of linear chromosomes[1][4][7]. This homeostatic mechanism primarily depends on the reverse transcriptase enzyme telomerase, which synthesizes telomeric repeats, and a specialized protein complex known as shelterin that protects chromosome ends and regulates access to telomerase[1][2][3][4][6]. Additional regulatory layers include epigenetic modifications and DNA damage response pathways[1][4][7]. Proper telomere maintenance is vital for chromosome stability, sustained cell division, and prevention of genomic instability. Disruption in telomere maintenance is implicated in cancer (where maintenance is often upregulated to allow unlimited division), premature aging syndromes, and degenerative diseases[2][5][8]. Dysfunction may arise from inherited mutations in telomerase or shelterin complex genes. Drugs do not typically interact with "telomere maintenance" as a single target; rather, compounds may modulate components of this system, such as telomerase inhibitors (e.g., imetelstat) or, experimentally, drugs targeting shelterin proteins or related pathways. Thus, telomere maintenance itself is not a discrete biomolecular entity but an ensemble process and regulatory network[1][2][7][10].
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