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Hereditary blockade of this DDR pathway, upon knockout of the Mb21d1 gene encoding CGAS, prolonged survival, improved cardiac function, partly restored quantities of molecular markers of heart failure, and attenuated myocardial apoptosis and fibrosis within the LMNA-deficient mice. The conclusions indicate that focusing on the CGAS/DDR path may be useful when you look at the treatment of DCM caused by mutations in
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