Key result
PDE1C inhibition or deficiency attenuated doxorubicin-induced cardiac toxicity and dysfunction in mice, a protective effect that was significantly diminished by A2R antagonism.
A novel multiprotein complex comprising A2R, PDE1C, and TRPC3 regulates cardiomyocyte survival, suggesting that targeting these molecules may protect against doxorubicin-induced cardiotoxicity.
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May identify PDE1C inhibition as protective in doxorubicin cardiotoxicity; hypothesis-generating from animal data only.
Zhang et al. (2018) studied Doxorubicin-induced cardiotoxicity and cardiomyocyte apoptosis. PDE1C inhibition or deficiency was evaluated on Cardiomyocyte death/apoptosis and cardiac toxicity. PDE1C inhibition or deficiency attenuated doxorubicin-induced cardiac toxicity and dysfunction in mice, a protective effect that was significantly diminished by A2R antagonism.
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