Identification of the molecular basis of doxorubicin-induced cardiotoxicity

By Sui Zhang, Xiaobing Liu, Tasneem Bawa-Khalfe, Long-Sheng Lu, Y. Lyu, Leroy F. Liu, E. Yeh. Nature Medicine, 2012

1,800 citations recorded by the source corpus.

Subfields: Cardiology and Cardiovascular Medicine, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/1e36569e95463c5020c0cf2f368fb8754e34ccc7

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cardiology and Cardiovascular Medicine

1. L. Badano
2. D. Lenihan
3. T. Marwick
4. P. Lancellotti
5. T. Force

In Molecular Biology

1. Steven Henikoff
2. Christopher Kemp
3. Sheila S. Teves
4. Fan Yang
5. T. Force
6. Pauline Crystal Ng
7. Burkhard Rost
8. Yana Bromberg

In Oncology

1. Steven Henikoff
2. Christopher Kemp
3. Sheila S. Teves
4. Fan Yang

Citations in the corpus

• Cardiotoxicity of doxorubicin is mediated through mitochondrial iron accumulation. (2014, neutral): “Although both studies reported significant and almost complete protection against DOX toxicity, our study design and protocol of DOX administration differ from those of Zhang et al., and thus we were unable to directly compare relative contributions of mitochondrial iron and Top-2 β deletion to card”
• Prevention of anthracycline-induced cardiotoxicity: challenges and opportunities. (2014, background): “Top2b is required for p53 activation in response to anthracycline-induced DNA damage in cardiomyocytes (18), whereas anthracycline-induced ROS production is due to a reduction in antioxidant enzyme gene transcription, which is also Top2bdependent (18).”
• Cardiotoxicity of anticancer treatments: Epidemiology, detection, and management (2016, background): “In addition, mechanisms have been identified, including disturbances in DNA topoisomerase 2-b (Top2b) metabolism.(25) The risk of doxorubicin-induced HF (which can occur within hours, weeks, or years after exposure) increases with cumulative dose of anthracycline: 3% to 5% with 400 mg/m(2), 7% to 26”
• Anthracycline Chemotherapy and Cardiotoxicity (2017, background): “Animal studies with Top2β knockout (KO) mice have shown that the absence of Top2β protects against doxorubicin-induced cardiotoxicity [24, 25] partially due to reduced mitochondrial dysfunction [25].”
• Mitochondria-dependent ferroptosis plays a pivotal role in doxorubicin cardiotoxicity (2020, neutral): “of DIC in the mice used in previous studies (3, 4), and no mice in our study died even at the 1-month period during which we monitored DIC progression.”
• Doxorubicin, DNA torsion, and chromatin dynamics (2013, positive): “Indeed, cardiomyocyte-specific deletion of topoisomerase IIβ has been shown to protect mice from developing doxorubicininduced heart failure [19].”
• Expert consensus for multimodality imaging evaluation of adult patients during and after cancer therapy: a report from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. (2014, background): “changes responsible for defective mitochondrial biogenesis, and reactive oxygen species formation.(8) The damage caused by the anthracyclines occurs in a cumulative dose-dependent fashion.”
• Redox regulation of FoxO transcription factors (2015, background): “Doxorubicin is an anthraquinone derivative, DNA intercalating agent and topoisomerase inhibitor known to generate ROS (although probably not through redox cycling of the quinone moiety) in cells [76].”
• Expert consensus for multimodality imaging evaluation of adult patients during and after cancer therapy: a report from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. (2014, background): “These complexes induce deoxyribonucleic acid double-strand breaks and transcriptome changes responsible for defective mitochondrial biogenesis, and reactive oxygen species formation.(8) The damage caused by the anthracyclines occurs in a cumulative dose–dependent fashion.”