Impaired End Joining Induces Cardiac Atrophy in a Hutchinson–Gilford Progeria Mouse Model

Using a GFP-based reporter system, the authors demonstrated that the efficiency of nonhomologous end joining declined by 50% in Hutchinson–Gilford progeria syndrome (HGPS) cardiomyocytes in vivo, due to the attenuated interaction between γH2AX and Progerin, the causative factor of HGPS.