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Anthracycline-induced cardiotoxicity: overview of studies examining the roles of oxidative stress and free cellular iron.
TLDR
Several lines of evidence suggest that mechanisms other than the traditionally emphasized "ROS and iron" hypothesis are involved in anthracycline-induced cardiotoxicity and that these alternative mechanisms may be better bases for designing approaches to achieve efficient and safe cardioprotection.
Oxidative stress, redox signaling, and metal chelation in anthracycline cardiotoxicity and pharmacological cardioprotection.
TLDR
Dexrazoxane may be the key to the enigma of anthracycline cardiotoxicity, and therefore it warrants further investigation, including the search for alternative/complementary modes of cardioprotective action beyond simple iron chelation.
Anthracycline-induced cardiotoxicity.
TLDR
Modification of dosage schedule and synthesis of new anthracycline analogues may represent alternative approaches to mitigate anthrACYcline cardiotoxicity while preserving antitumour activity.
SIH--a novel lipophilic iron chelator--protects H9c2 cardiomyoblasts from oxidative stress-induced mitochondrial injury and cell death.
TLDR
Iron chelation is presented as a very powerful tool by which oxidative stress-induced myocardial damage can be prevented.
Molecular Remodeling of Left and Right Ventricular Myocardium in Chronic Anthracycline Cardiotoxicity and Post-Treatment Follow Up
Chronic anthracycline cardiotoxicity is a serious clinical issue with well characterized functional and histopathological hallmarks. However, molecular determinants of the toxic damage and associated
Proteomic insights into chronic anthracycline cardiotoxicity.
TLDR
For the first time, the complex proteomic signature of chronic anthracycline cardiotoxicity was revealed which enhances understanding of the basis for this phenomenon and it may enhance efforts in targeting its reduction.
In vitro and in vivo examination of cardiac troponins as biochemical markers of drug-induced cardiotoxicity.
TLDR
The release kinetics of cardiac troponin T and cTnI are confirmed as very sensitive and specific markers of anthracycline-induced cardiomyopathy in vivo and can become not only the bridge between the clinical and experimental studies of drug- induced cardiotoxicity but also the linkage between the preclinical experiments in vitro and in vivo.
Cardioprotective Effects of a Novel Iron Chelator, Pyridoxal 2-Chlorobenzoyl Hydrazone, in the Rabbit Model of Daunorubicin-Induced Cardiotoxicity
TLDR
It is shown that shielding of free intracellular iron using a potent lipophilic iron chelator is able to offer a meaningful protection against chronic anthracycline cardiotoxicity, which suggests that iron might play more complex role in the pathogenesis of this disease than previously assumed.
Rabbit model for in vivo study of anthracycline‐induced heart failure and for the evaluation of protective agents
Cardiac toxicity associated with chronic administration of anthracycline (ANT) antibiotics represents a serious complication of their use in anticancer chemotherapy, but can also serve as a useful
Toxicities of O-alkyl S-(2-dialkylaminoethyl) methyl phosphonothiolates (V-compounds).
TLDR
Rats were more sensitive to these compounds than mice, rabbits and guinea-pigs were moresensitive than mice and rats, and the most sensitive toThese compounds were dogs.
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