Abstract
Telomeres, located at the end of chromosomes to maintain their integrity, are a major focus of aging research as (1) a small portion of telomeric DNA is lost with each cell division, (2) they are shortened by oxidative damage and (3) when telomere length reaches a critical limit, cells enter a senescence state and/or apoptosis (Simons 2015). Telomere length may serve as a biological clock to determine the lifespan of a cell and an organism (Shammas 2011), as pioneer experiments demonstrated that telomere length predicts the in vitro replicative capacity of human fibroblasts and that overexpressing telomerase immortalizes fibroblasts in cell cultures (Bodnar et al. 1998, Rudolph et al. 1999). It was later demonstrated that in vivo human telomeres shorten during aging (Muezzinler et al. 2013).
Original language | English (US) |
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Title of host publication | Mechanisms Linking Aging, Diseases and Biological Age Estimation |
Publisher | CRC Press |
Pages | 141-149 |
Number of pages | 9 |
ISBN (Electronic) | 9781498709705 |
ISBN (Print) | 9781498709699 |
DOIs | |
State | Published - Jan 1 2017 |
Externally published | Yes |
All Science Journal Classification (ASJC) codes
- General Social Sciences
- General Medicine
- General Biochemistry, Genetics and Molecular Biology
Keywords
- Aging
- Aging-associated diseases
- Hayflick limit
- Heritable trait
- Lifespan
- Oxidative stress
- Progeroid syndromes
- Senescence
- Telomerase
- Telomere length
- Telomere rate of change (troc)
- Telomere shortening (attrition)