Reducing nuclei damage improves heart function and survival in mice - Cornell Chronicle
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Reducing damage to the nuclei of heart muscle cells improved heart function and dramatically extended survival in mice with a form of inherited heart disease, according to a new study led by Cornell researchers. The findings point to new approaches for understanding and potentially treating LMNA-related dilated cardiomyopathy, a disease that leads to heart failure and sudden cardiac death. The study, published in Circulation Research, was directed by Jan Lammerding, a professor in the Meinig School of Biomedical Engineering in the Cornell Duffield College of Engineering and a member of the Weill Institute for Cell and Molecular Biology, and jointly led by Noam Zuela-Sopilniak and Julien L. P. Morival in his group. Co-corresponding author Iwijn De Vlaminck is also a professor in the Meinig School. LMNA-related dilated cardiomyopathy is an inherited heart disease caused by mutations in the LMNA gene, which encodes lamin A and lamin C, proteins that help maintain the structural integrity of a cell’s nucleus. Although researchers have identified a link between LMNA mutations and heart disease, they do not completely understand the cellular mechanisms that lead to heart damage.
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