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Cited by 297

The DOI matches its Crossref record; 14 of the 14 references it cites were found in a registry or an index.

Doxorubicin-induced reactive oxygen species generation and intracellular Ca2+increase are reciprocally modulated in rat cardiomyocytes

Open access
Kim, Seon-Young, Kim, Sang-Jin, Kim, Byoung-Joo, Rah, So-Young, Chung, Sung Mo, Im, Mie-Jae, Kim, Uh-Hyun·2006·Experimental & Molecular Medicine
DOI 10.1038/emm.2006.63
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Abstract

Doxorubicin (DOX) is one of the most potent anticancer drugs and induces acute cardiac arrhythmias and chronic cumulative cardiomyopathy. Though DOX-induced cardiotoxicity is known to be caused mainly by ROS generation, a disturbance of Ca2+ homeostasis is also implicated one of the cardiotoxic mechanisms. In this study, a molecular basis of DOX-induced modulation of intracellular Ca2+ concentration ([Ca2+]i) was investigated. Treatment of adult rat cardiomyocytes with DOX increased [Ca2+]i irrespectively of extracellular Ca2+, indicating DOX-mediated Ca2+ release from intracellular Ca2+ stores. The DOX-induced Ca2+ increase was slowly processed and sustained. The Ca2+ increase was inhibited by pretreatment with a sarcoplasmic reticulum (SR) Ca2+ channel blocker, ryanodine or dantrolene, and an antioxidant, alpha-lipoic acid or alpha-tocopherol. DOX-induced ROS generation was observed immediately after DOX treatment and increased in a time-dependent manner. The ROS production was significantly reduced by the pretreatment of the SR Ca2+ channel blockers and the antioxidants. Moreover, DOX-mediated activation of caspase-3 was significantly inhibited by the Ca2+ channel blockers and a-lipoic acid but not a-tocopherol. In addition, cotreatment of ryanodine with alpha-lipoic acid resulted in further inhibition of the casapse-3 activity. These results demonstrate that DOX-mediated ROS opens ryanodine receptor, resulting in an increase in [Ca2+]i and that the increased [Ca2+]i induces ROS production. These observations also suggest that DOX/ROS-induced increase of [Ca2+]i plays a critical role in damage of cardiomyocytes.

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Metadata

Authors
Kim, S.-Y., Kim, S.-J., Kim, B.-J., Rah, S.-Y., Chung, S. M., Im, M.-J., & Kim, U.-H.
Venue
Experimental & Molecular Medicine
Publisher
Springer Science and Business Media LLC
Published
2006-10-01
Volume
38
Issue
5
Pages
535-545
ISSN
  • 1226-3613 (ISSN-L)
  • 2092-6413
DOI
10.1038/emm.2006.63
OpenAlex
W1964179489
Cited by
297
References
14
FWCI
5.03
Type
journal article
Language
en
Open access
gold

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