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Inhibition of CACNA1H attenuates doxorubicin-induced acute cardiotoxicity by affecting endoplasmic reticulum stress.

08:00 EDT 30th September 2019 | BioPortfolio

Summary of "Inhibition of CACNA1H attenuates doxorubicin-induced acute cardiotoxicity by affecting endoplasmic reticulum stress."

Doxorubicin (DOX) is an anticancer drug that has been widely used in the clinic. However, recently its application has been limited due to the cardiotoxic effects it has caused. Severe cardiotoxicity of DOX causes cardiac hypertrophy that may lead to heart failure. It has previously been demonstrated that CACNA1H is re-expressed in hypertrophic cardiomyocytes. In this study, we aimed to investigate the role of CACNA1H in DOX-induced acute cardiotoxicity, and to investigate its possible underlying mechanisms of action involved.

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This article was published in the following journal.

Name: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
ISSN: 1950-6007
Pages: 109475

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