Oxidative stress shortens telomeres.
By T. von Zglinicki. TIBS -Trends in Biochemical Sciences. Regular ed, 2002
2,480 citations recorded by the source corpus.
Subfields: Aging, Physiology
View Paper: https://www.semanticscholar.org/paper/ead8c9570ffc6b996238dc1f13e9959422021920
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Aging
- Mark Ferreira
- Thomas B. L. Kirkwood
- N. Marchetto
- M. Haussmann
- J. Passos
- U. Herbig
- John M. Sedivy
- J. Campisi
In Physiology
- John M. Sedivy
- Mark Ferreira
- Thomas B. L. Kirkwood
- N. Marchetto
- M. Haussmann
- J. Passos
- Glyn Nelson
- U. Herbig
Citations in the corpus
- Accumulation of senescent cells in mitotic tissue of aging primates. (2007, background): “Factors such as reactive oxygen species (ROS) (von Zglinicki, 2002), nucleases (Lydall, 2003), secondary structures in telomeric DNA (Ding et al., 2004) and sporadic loss of large telomeric stretches (Wang et al., 2004) have all been implicated to contribute to telomere erosion and telomere…”
- Telomere length, non-breeding habitat and return rate in male American redstarts (2013, background): “These constraints could induce greater oxidative stress and, thus, explain why telomeres shorten at a greater rate in scrub-habitat birds than mangrove-habitat birds as oxidative stress is a major determinant of telomere shortening (Von Zglinicki 2002).”
- Oxidative Stress in Aging Human Skin (2015, neutral): “arrest of cells [343,344].”
- Telomeres: Linking stress and survival, ecology and evolution (2010, background): “In human cells, telomeres shorten by 50–300 base pairs per cell division (Harley et al., 1990; Aubert et al., 2008), but only approximately ten base pairs of this reduction is thought to be due to the end-replication problem (von Zglinicki, 2002).”
- Mitochondrial Dysfunction Accounts for the Stochastic Heterogeneity in Telomere-Dependent Senescence (2007, methodology): “negative human somatic cells can be significantly modulated by either increasing oxidative stress [10] or by antioxidant protection [34,37].”
- Mitochondrial dysfunction in cell senescence and aging (2022, background): “This increase in oxidative stress leads to DNA damage, such as oxidized bases, single-strand breaks, double-strand breaks, and telomere shortening (4), activating p53 and pRb pathways and causing cell cycle arrest and senescence (28, 108).”
- Telomeres and telomerase. (2002, neutral): “But, for example, variable levels of oxidative stress correlate with increased telomere shortening rates (Von Zglinicki 2002).”
- Aging, Cellular Senescence, and Cancer (2012, neutral): “Oxidative stress can also accelerate telomere shortening (40), presumably because the G-rich telomeric DNA is particularly vulnerable to oxidative damage.”
- Protocols to detect senescence-associated beta-galactosidase (SA-βgal) activity, a biomarker of senescent cells in culture and in vivo (2009, neutral): “The telomere shortening observed did not reach the critical telomere shortening described for replicative senescenc”
- Impact of Urbanization on Birds (2018, neutral): “Another aging biomarker that may be linked to oxidative stress is the shortening of telomeres (von Zglinicki 2002; Boonekamp et al. 2017).”
- Growing in Cities: An Urban Penalty for Wild Birds? A Study of Phenotypic Differences between Urban and Rural Great Tit Chicks (Parus major) (2017, neutral): “Telomeres usually shorten as individual age, and importantly, environmental stressors and the occurrence of oxidative stress have been shown to accelerate this shortening (von Zglinicki, 2002).”