Impaired end joining induces cardiac atrophy in a Hutchinson–Gilford progeria mouse model

Abstract excerpt

Patients with Hutchinson–Gilford progeria syndrome (HGPS) present with a number of premature aging phenotypes, including DNA damage accumulation, and many of them die of cardiovascular complications. Although vascular pathologies have been reported, whether HGPS patients exhibit cardiac dysfunction and its underlying mechanism is unclear, rendering limited options for treating HGPS-related cardiomyopathy. In this...

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