Cardiotoxicity of doxorubicin is mediated through mitochondrial iron accumulation.

By Y. Ichikawa, Mohsen Ghanefar, Marina Bayeva, Rongxue Wu, Arineh Khechaduri, S. N. Prasad, R. Mutharasan, Tejaswitha Jairaj, Hossein Naik, Ardehali and 2 more. Journal of Clinical Investigation, 2014

802 citations recorded by the source corpus.

Subfields: Biophysics, Cardiology and Cardiovascular Medicine, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/a1f800b6e7510366642dd2a40802a28cd5869bc9

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In Molecular Biology

1. W. Gu
2. Hiroyuki Tsutsui
3. J. Min

Citations in the corpus

• Mitochondria-dependent ferroptosis plays a pivotal role in doxorubicin cardiotoxicity (2020, positive): “Although some studies demonstrated that iron chelation using DXZ ameliorated DIC in a mouse model (5, 42), we speculate that long-term treatment with DXZ in vivo might be effective for DIC, possibly irrespective of ferroptosis.”
• Ferroptosis as a target for protection against cardiomyopathy (2019, background): “On the other hand, a growing body of evidence indicates that increased iron may play a key role in this condition (15), but the fundamental mechanisms of iron accumulation and its toxicity are poorly understood.”
• Anthracycline Chemotherapy and Cardiotoxicity (2017, background): “and potentiating ferrous-ferric cycling of molecular iron [17].”
• Ferroptosis in cancer: from molecular mechanisms to therapeutic strategies (2024, background): “114 Moreover, ferroptosis is also implicated in radiation-induced intestinal injury, which can be alleviated by administering ferrostatin-1.”