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Genotoxic cancer therapies are known to be potent drivers of cardiomyopathy, whereas causes of spontaneous disease remain unclear. To test the hypothesis that endogenous genotoxic stress contributes to cardiomyopathy, we deleted the DNA repair gene\n                    <jats:italic>Ercc1<\/jats:italic>\n                    specifically in striated muscle using a floxed allele of\n                    <jats:italic>Ercc1<\/jats:italic>\n                    and mice expressing Cre under control of the muscle\u2010specific creatinine kinase (\n                    <jats:italic>Ckmm<\/jats:italic>\n                    ) promoter or depleted systemically (\n                    <jats:italic>Ercc1<\/jats:italic>\n                    <jats:sup>\u2212\/D<\/jats:sup>\n                    mice).\n                    <jats:italic>Ckmm\u2010Cre<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>+\/\u2212<\/jats:italic>\n                    <\/jats:sup>\n                    <jats:italic>;Ercc1<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2212\/fl<\/jats:italic>\n                    <\/jats:sup>\n                    mice expired suddenly of heart disease by 7 months of age. As young adults, the hearts of\n                    <jats:italic>Ckmm\u2010Cre<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>+\/\u2212<\/jats:italic>\n                    <\/jats:sup>\n                    <jats:italic>;Ercc1<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2212\/fl<\/jats:italic>\n                    <\/jats:sup>\n                    mice were structurally and functionally normal, but by 6\u2010months\u2010of\u2010age, there was significant ventricular dilation, wall thinning, interstitial fibrosis, and systolic dysfunction indicative of dilated cardiomyopathy. Cardiac tissue from the tissue\u2010specific or systemic model showed increased apoptosis and cardiac myocytes from\n                    <jats:italic>Ckmm\u2010Cre<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>+\/\u2010<\/jats:italic>\n                    <\/jats:sup>\n                    <jats:italic>;Ercc1<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2212\/fl<\/jats:italic>\n                    <\/jats:sup>\n                    mice were hypersensitive to genotoxins, resulting in apoptosis. p53 levels and target gene expression, including several antioxidants, were increased in cardiac tissue from\n                    <jats:italic>Ckmm\u2010Cre<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>+\/\u2212<\/jats:italic>\n                    <\/jats:sup>\n                    <jats:italic>;Ercc1<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2212\/fl<\/jats:italic>\n                    <\/jats:sup>\n                    and\n                    <jats:italic>Ercc1<\/jats:italic>\n                    <jats:sup>\u2212\/D<\/jats:sup>\n                    mice. Despite this, cardiac tissue from older mutant mice showed evidence of increased oxidative stress. Genetic or pharmacologic inhibition of p53 attenuated apoptosis and improved disease markers. Similarly, overexpression of mitochondrial\u2010targeted catalase improved disease markers. Together, these data support the conclusion that DNA damage produced endogenously can drive cardiac disease and does so mechanistically via chronic activation of p53 and increased oxidative stress, driving cardiac myocyte apoptosis, dilated cardiomyopathy, and sudden death.\n                  <\/jats:p>","DOI":"10.1111\/acel.13782","type":"journal-article","created":{"date-parts":[[2023,2,3]],"date-time":"2023-02-03T04:35:33Z","timestamp":1675398933000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":28,"title":["Loss of\n                    <scp>DNA<\/scp>\n                    repair mechanisms in cardiac myocytes induce dilated cardiomyopathy"],"prefix":"10.1111","volume":"22","author":[{"given":"Chathurika","family":"Henpita","sequence":"first","affiliation":[{"name":"Department of Biochemistry, Molecular Biology and Biophysics, Institute on the Biology of Aging and Metabolism University of Minnesota  Minneapolis Minnesota 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