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As cells age, telomere length shortens, and mitochondrial function diminishes (respiratory-chain functions decrease, and production of reactive oxygen species increases). These cellular abnormalities have been associated with phenomena and diseases of aging such as muscle atrophy, age-related cardiomyopathy with left ventricular dysfunction, impaired glucose metabolism, and neurodegeneration. In a new study, researchers propose a molecular explanation that links these observations.
A team in Massachusetts genetically engineered mice that had various telomere lengths, ranging from normal (wild type) to very short. Expression of the p53 tumor-supressor gene and two other genes, PGC-1α and PGC-1β, was downregulated as telomere lengths became sh…