Telomere attrition refers to the process of gradual shortening of the telomeres, the protective caps at the ends of chromosomes.

Telomeres are made up of repetitive sequences of DNA and are crucial for maintaining the stability and integrity of the genome. They protect the ends of chromosomes from degradation, fusion with other chromosomes, and inappropriate recombination.

Every time a cell divides, its telomeres get slightly shorter due to the “end-replication problem,” where the DNA replication machinery cannot fully replicate the very ends of the linear DNA molecules. Over time and successive cell divisions, this leads to telomere attrition.

When telomeres reach a critically short length, they lose their protective function and the cell often enters a state of senescence (a type of permanent cell cycle arrest) or apoptosis (programmed cell death). This is a protective mechanism to prevent the propagation of cells with potential genomic instability. However, if these safety mechanisms are bypassed, cells with critically short telomeres may continue to divide, leading to further genomic instability and potentially contributing to the development of cancer.

Certain factors can accelerate telomere attrition, including oxidative stress, inflammation, and certain lifestyle factors such as poor diet, lack of exercise, smoking, and chronic psychological stress. In contrast, the enzyme telomerase can add DNA to the ends of chromosomes and counteract telomere attrition, but it is not active in most human cells.

Telomere attrition is also associated with aging and a number of age-related diseases. Research in this area is ongoing, with the aim of better understanding the role of telomeres in aging and disease, and potentially developing interventions to maintain telomere length and improve health.