telomerforkorting

Telomere shortening refers to the gradual loss of telomeric DNA repeats at the ends of linear chromosomes as cells divide. Telomeres protect coding regions from erosion and help maintain genomic stability. In most somatic cells, telomeres shorten with age, and when they reach a critical length, cells enter replicative senescence or undergo apoptosis.

Telomeres are maintained by the enzyme telomerase in stem and germ cells; most adult somatic cells have low or inactive telomerase. The shelterin protein complex protects chromosome ends, while the end-replication problem contributes to shortening. Some cancer cells employ alternative lengthening of telomeres (ALT) to maintain length.

Rate of shortening is influenced by genetics and environment. Inherited telomere biology disorders (e.g., dyskeratosis congenita) produce unusually short telomeres. Oxidative stress, inflammation, and high cellular turnover accelerate shortening. Lifestyle factors such as smoking, obesity, and chronic stress have been associated with shorter telomeres, though causality and effect sizes vary.

Associations exist between shorter telomeres and aging-related diseases, including cardiovascular disease, neurodegenerative disorders, and weakened immune function. It is debated whether telomere length is a causal driver of disease or a biomarker of cumulative cellular damage.

Measurement of telomere length is usually performed on leukocytes using methods such as quantitative PCR or Southern blot; results vary by tissue and method. Research explores interventions—energy balance, physical activity, stress reduction—although evidence for substantial lengthening of telomeres in humans is limited. Therapeutic approaches that activate telomerase raise concerns about cancer risk, and no approved anti-aging treatments target telomere length.