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Their study underscores the presence of a positive feedback between Wnt signaling and telomere function, whereby stimulation
of Wnt signaling activates expression of proteins that enhance the “cap” on telomeres, leading to more functional stem cells, which
in turn stimulates the Wnt pathway further.
The research also provides insights into strategies to combat telomere dysfunction, a process that has also been implicated in some cancers and natural aging.
“What you see in the mutant mice and the dyskeratosis congenita patients is the consequence of having less telomerase activity in rapidly dividing tissues,” said Johnson, co-senior author on the study and an associate professor of pathology and laboratory medicine in Penn Medicine. “It’s not the same thing as natural aging where you might have telomere defects in cells that don’t have a lot of telomerase activity to begin with. But I think it’s fair to say our findings inform an understanding of some of what might be happening as telomeres shorten in aging.”
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