Key result
Doxorubicin cuts cardiomyocyte viability up to ~53%, which NOX and MPO inhibitors attenuate.
Why the study?
Doxorubicin-induced cardiotoxicity involves mitochondrial dysfunction and oxidative stress, but the specific mechanisms of ROS generation in cardiomyocytes remain to be elucidated.
Population
H9c2 cardiomyocytes treated with 5 µM doxorubicin
Comparison
DOX treatment with or without inhibitors of NOX, MPO, mitochondrial oxidative phosphorylation, and ROS scavenger versus controls
Design
Preclinical experimental study using cell assays and inhibitors
Authors
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Supports NOX/MPO inhibition in doxorubicin cardiotoxicity models; hypothesis-generating and leaves open clinical translation.
p-value: p=<0.05
Doxorubicin-induced cardiotoxicity in H9c2 cardiomyocytes is critically mediated by ROS generated via NADPH oxidase and myeloperoxidase, leading to mitochondrial dysfunction and apoptosis.
Upadhayay et al. (2020) studied Doxorubicin-induced cardiotoxicity. Doxorubicin vs. Untreated control cells was evaluated on Cell viability and ROS generation (p=<0.05). Doxorubicin reduced cell viability by up to 53% and increased ROS levels in H9c2 cardiomyocytes, leading to mitochondrial dysfunction and apoptosis that was attenuated by NOX and MPO inhibitors.
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