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Doxorubicin is a widely used chemotherapeutic agent that causes severe acute or chronic cardiomyopathy and congestive heart failure, particularly at high doses or in high-risk populations.
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This editorial discusses the mechanisms of doxorubicin-induced cardiomyopathy and congestive heart failure, specifically referencing the role of AMPK signaling inhibition.
This editorial refers to ‘Inhibition of AMPK signalling by doxorubicin: at the crossroads of the cardiac responses to energetic, oxidative, and genotoxic stress’ by S. Gratia et al., pp. 290–299, this issue. Doxorubicin (DXR) is one of the most widely used chemotherapeutics in the treatment of a variety of cancers, including breast, prostate, stomach and liver tumours, soft tissue sarcomas, leukaemias, and lymphomas.1 The anti-malignancy effects of DXR are attributed to its interaction with the DNA helix and proteins involved in DNA replication and transcription, resulting in the inhibition of synthesis of DNA, RNA, and proteins and ultimately cell death.2 However, DXR causes severe cardiomyopathy and resultant congestive heart failure, especially in patients treated with a high dose or in high-risk populations such as children, adolescents, or patients with predisposed cardiac problems. DXR-induced cardiac injury is manifested as acute or chronic cardiomyopathy, and both can eventually develop into severe congestive heart failure.
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Zhang et al. (2012) conducted an editorial in Doxorubicin-induced cardiomyopathy. Doxorubicin was evaluated. Doxorubicin is a widely used chemotherapeutic agent that causes severe acute or chronic cardiomyopathy and congestive heart failure, particularly at high doses or in high-risk populations.
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