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Under conditions of severe DNA damage, PARP hyperactivation can deplete cellular NAD+ pools, reducing sirtuin activity and mitochondrial function while promoting cell death through energy depletion

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These therapies display higher efficiency compared to classical senolytic drugs (BCL-2 or tyrosine kinase inhibitors) but for some of them, such as NA + /K + ATPase inhibitors, clinical development could be complex in the light of strong cardiotoxicity associated with this class of molecules

doi:10.1046/j.1523-1747.1999.00606.x