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Model for the activation of robust cardiotoxic genes during doxorubicin-induced cardiotoxicity. Dox treatment increases the deposition of H3K27ac at promoters of robust cardiotoxic genes, and activates their transcription in cardiomyocytes. These results further promote DNA damage in the nucleus, and excessive genome instability leads to heart failure. C646 treatment reduces the expression of doxorubicin-induced cardiotoxic genes, and improves the cardiac function
