A huge game changer:
Aging is generally accompanied by a gradual decline in cellular and organ functioning that eventually results in increased mortality risk. One proposed mechanism for aging focuses on telomere maintenance. Telomeres are the ends of chromosomes that, for mechanical reasons, require a special copying enzyme. Human germ cells produce a complex called telomerase to maintain telomere length; other human cells do not. As a result, the telomeres of most cells get shorter with each cell division. Eventually, their reduced length activates DNA damage signaling pathways that induce the cell to enter a sort of senescence.
Interestingly, mouse somatic cells express telomerase and therefore do not senesce in culture. So, to provide models for humans, we had to genetically engineer mice that lack telomerase. These mice display widespread tissue atrophy, especially in highly proliferative organs like the spleen, intestines, and testes. They also suffer from loss of germ cells, stem cell depletion, organ system failure, impaired tissue injury response, and a lifespan diminished by half.
The rest is here:
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