Loss of Repressor Activator Protein 1 Precipitates Cardiac Aging in Mice via p53/PPARα Signaling
April 2020
in “
The FASEB Journal
”
Studysummary This study found that Rap1 deficiency in mice may lead to telomere shortening, DNA damage, and impaired mitochondrial function, contributing to cardiac aging and dysfunction.
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The study investigated the role of repressor activator protein 1 (Rap1) in cardiac aging in mice, revealing that Rap1 deficiency led to pronounced aging-related cardiac dysfunction. This was evidenced by structural changes, reduced cardiac function, and mitochondrial abnormalities. Mechanistically, the loss of Rap1 resulted in shorter telomeres, increased DNA damage, and elevated p53 levels, which suppressed PPARα, impairing fatty acid metabolism (FAM). Treatment with a p53 inhibitor alleviated these effects, suggesting that Rap1 plays a crucial role in maintaining cardiac health by regulating telomere integrity and mitochondrial function. The study highlighted a potential new dimension in the physiological role of telomere-Rap1 in cardiac aging.
