Review examines conflicting evidence on leukocyte telomere shortening in mice, highlighting implications for modeling human aging-related diseases.
In most actively dividing human somatic cells, telomeres shorten with age. Their shortening drives the aging of tissues leading, ultimately, to death. Age-dependent leukocyte telomere shortening is associated with aging-related diseases in humans and decreased lifespan in other animals. A recent study has unexpectedly realized that telomeres do not shorten with age in the mouse tail and leukocytes. In the present article, we discuss the potential implications of these seemingly conflicting results. We propose that further research should uncover the factors determining the shortening (or not) of leukocyte telomeres. This approach could help to understand the pathophysiology of human diseases related to inadequate telomere length in leukocytes.
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Pessoa et al. (2026) studied this question.
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