Question: Is Doxorubicin cardiotoxic?

Context:
Doxorubicin (DOXO) is widely used to treat solid tumors. However, its clinical use is limited by side effects including serious cardiotoxicity due to cardiomyocyte damage. 
The results provide direct evidence for the role of catalase in doxorubicin cardiotoxic responses.
These results do not support the possibility that mitomycin C potentiates the acute cardiotoxic effects produced by doxorubicin.
The anthracycline chemotherapeutic agent doxorubicin is converted by the enzyme carbonyl reductase 1 (CBR1) into its cardiotoxic metabolite doxorubicinol
The clinical efficiency of the highly potent antitumor agent doxorubicin is limited by cardiotoxic effects
Doxorubicin (DOX), a highly active chemotherapeutic drug, faces limitations in clinical application due to severe cardiotoxic effects (mainly through increased oxidative stress)
Clinical uses of doxorubicin (DOX), a highly active anticancer agent, are limited by its severe cardiotoxic side effects associated with increased oxidative stress and apoptosis
Doxorubicin (DOX) and trastuzumab (TRZ) are highly effective chemotherapeutic agents in the breast cancer setting, limited by their cardiotoxic side effects
Twisting and ironing: doxorubicin cardiotoxicity by mitochondrial DNA damage.
Cardiotoxic effects were reported in 15 (5%) of 291 children receiving treatment including doxorubicin.
On the other hand, pretreatment of rats with hesperidin protected cardiac tissues against the cardiotoxic effects of doxorubicin as evidenced from amelioration of histopathological changes and normalization of cardiac biochemical parameters.Hesperidin may have a protective effect against DOX-induced cardiotoxicity.
However, with cumulative doses, doxorubicin also is known to have cardiotoxic effects, including cardiomyopathy and heart failure.
Methods of reducing or preventing doxorubicin-induced cardiotoxicity have been suggested, including an investigational doxorubicin analog, mitoxantrone ( Novantrone ).
The most cardiotoxic drug, doxorubicin, is the most potent inducer of superoxide generation, while epirubicin, which is less cardiotoxic, has a relatively limited effect on superoxide production.
The mechanism of doxorubicin cardiotoxicity is likely multifactorial and most importantly, the genetic factors predisposing to doxorubicin cardiotoxicity are unknown.
As doxorubicin cardiotoxicity is considered irreversible, early detection of cardiotoxicity and prevention of overt heart failure is essential.
Although there are monitoring guidelines for cardiotoxicity, optimal timing for early detection of subclinical doxorubicin cardiotoxicity is still obscure.
Quercetin attenuates doxorubicin cardiotoxicity by modulating Bmi-1 expression.
However, doxorubicin cardiotoxicity of the heart has largely limited its clinical use.
Mitochondrial topoisomerase I (top1mt) is a novel limiting factor of doxorubicin cardiotoxicity.
Doxorubicin-based chemotherapy induces cardiotoxicity, which limits its clinical application.
he clinical use of doxorubicin (DOX) and other anthracyclines is limited by a dosage-dependent cardiotoxicity, which can lead to cardiomyopathy. 
Besides its cardiotoxic effect, doxorubicin also elicits inflammatory effects in vivo. 7-Monohydroxyethylrutoside (monoHER) has recently been used as a protector against doxorubicin-induced cardiotoxicity in vivo.
Doxorubicin is an effective antineoplastic agent, but it frequently causes dose-related cardiotoxic effects. 
Among these analogs, idarubicin (4-demethoxy-daunorubicin) was shown to be less cardiotoxic than doxorubicin i
Verapamil has also been suggested to potentiate the cardiotoxicity of doxorubicin. 
Doxorubicin treatment is associated with both acute and chronic cardiotoxicity. 
cardiac effects of diclofenac sodium on doxorubicin-induced cardiomyopathy in rats

Answer: Doxorubicin (DOXO) is widely used to treat solid tumors. However, its clinical use is limited by side effects including serious cardiotoxicity due to cardiomyocyte damage
Doxorubicin (DOXO) is widely used to treat solid tumors. However, its clinical use is limited by side effects including serious cardiotoxicity due to cardiomyocyte damage. 
Exact answer: yes