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• W3204047887 abstract "Late cardiac toxicity is a potentially lethal complication of cancer therapy, yet the pathogenic mechanism remains largely unknown, and few treatment options exist. Here we report DNA damaging agents such as radiation and anthracycline chemotherapies induce delayed cardiac inflammation following therapy due to activation of cGAS and STING-dependent type I interferon signaling. Genetic ablation of cGAS-STING-signaling in mice inhibits DNA damage induced cardiac inflammation, rescues late cardiac functional decline, and prevents death from cardiac events. Treatment with a STING antagonist suppresses cardiac interferon signaling following DNA damaging therapies and effectively mitigates cardiotoxicity. These results identify a therapeutically targetable, pathogenic mechanism for one of the most vexing treatment-related toxicities in cancer survivors." @default.
• W3204047887 created "2021-10-11" @default.
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• W3204047887 date "2021-09-26" @default.
• W3204047887 modified "2023-09-27" @default.
• W3204047887 title "Innate immune signaling drives late cardiac toxicity following DNA damaging cancer therapies" @default.
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• W3204047887 doi "https://doi.org/10.1101/2021.09.26.461865" @default.
• W3204047887 hasPublicationYear "2021" @default.
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