Journal
MECHANISMS OF AGEING AND DEVELOPMENT
Volume 177, Issue -, Pages 37-45Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mad.2018.03.013
Keywords
Telomeres; Oxidative stress; Oxidative DNA damage; Base excision repair
Categories
Funding
- National Institute of Environmental Health [ES R01ES022944, R21/33ES025606, ES028242]
- National Institute of General Medicine [R43GM108187]
- National Cancer Institute [CA207342]
- NATIONAL CANCER INSTITUTE [R01CA207342] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [R01ES022944, R01ES028242, R33ES025606, R21ES025606] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R44GM108187, R43GM108187] Funding Source: NIH RePORTER
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Telomeres are dynamic nucleoprotein-DNA structures that cap and protect linear chromosome ends. Because telomeres shorten progressively with each replication, they impose a functional limit on the number of times a cell can divide. Critically short telomeres trigger cellular senescence in normal cells, or genomic instability in pre-malignant cells, which contribute to numerous degenerative and aging-related diseases including cancer. Therefore, a detailed understanding of the mechanisms of telomere loss and preservation is important for human health. Numerous studies have shown that oxidative stress is associated with accelerated telomere shortening and dysfunction. Oxidative stress caused by inflammation, intrinsic cell factors or environmental exposures, contributes to the pathogenesis of many degenerative diseases and cancer. Here we review the studies demonstrating associations between oxidative stress and accelerated telomere attrition in human tissue, mice and cell culture, and discuss possible mechanisms and cellular pathways that protect telomeres from oxidative damage.
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