Reducing nuclear damage improves heart function and survival in mice
Reducing damage to the nuclei of heart muscle cells improved heart function and 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.
A new study led by Cornell researchers reveals that mitigating damage to heart muscle cell nuclei can restore heart function and extend survival in mice with LMNA-related dilated cardiomyopathy. The disease, caused by mutations in the LMNA gene, results in heart failure and sudden death. By targeting the LINC complex, which transmits mechanical forces from the cell to the nucleus, researchers were able to prevent nuclear rupture and associated inflammatory signaling.
This intervention restored nearly normal cardiac function and doubled the lifespan of the mice. The findings suggest that reducing nuclear damage could be a viable strategy for treating not only inherited heart disease, but also other forms of cardiac dysfunction, including those caused by aging or myocardial infarction.
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