Why the study?
Doxorubicin is a potent chemotherapeutic agent known to induce cardiotoxicity, but its derangement of cardiac dynamics needed investigation.
Does doxorubicin alter calcium transient and sarcomere contraction in a zebrafish model?
Does doxorubicin alter calcium transient and sarcomere contraction in a zebrafish model?
One-dimensional scanning multiphoton imaging reveals that doxorubicin prolongs the restoration phase of calcium transients and delays sarcomere relaxation in a zebrafish model, suggesting impaired calcium recycling as a mechanism of cardiotoxicity.
Should not yet change DOX cardiotoxicity practice; leaves open whether this zebrafish phenotype translates to human anthracycline injury.
Doxorubicin (DOX) is a potent chemotherapeutic agent known to induce cardiotoxicity. Here we applied one-dimensional scanning multiphoton imaging to investigate the derangement of cardiac dynamics induced by DOX on a zebrafish model. DOX changed the cell morphology and significantly prolonged calcium transient and sarcomere contraction, leading to an arrhythmia-like contractile disorder. The restoration phase of calcium transient dominated the overall prolongation, indicating that DOX perturbed primarily the protein functions responsible for recycling cytosolic calcium ions. This novel finding supplements the existing mechanism of DOX cardiotoxicity. We anticipate that this approach should help mechanistic studies of drug-induced cardiotoxicity or heart diseases.
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Chao et al. (2021) studied this question.
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