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Oxidative stress therefore accelerates telomere shortening beyond the end-replication problem alone, creating a feed-forward loop in which mitochondrial dysfunction generates reactive oxygen species (ROS) that damage telomeres, triggering senescence and further mitochondrial dysfunction
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Is there a better 'treat' to give them
Gender and sex differences in adipose tissue
PD-1 regulates KLRG1(+) group 2 innate lymphoid cells
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