Key result
Inhibition of miR-375 prevented doxorubicin-induced oxidative stress and cardiomyocyte apoptosis in vivo and in vitro through the PDK1/AKT signaling pathway.
Why the study?
Inhibition of miR-375 reduces inflammation and increases cardiomyocyte survival, prompting investigation of its effects and mechanisms in doxorubicin-induced cardiac toxicity.
Does inhibition of miR-375 prevent oxidative damage and apoptosis in a mouse model of doxorubicin-induced cardiac toxicity?
Population
Mouse model of doxorubicin-induced cardiac toxicity and cultured rat and mouse cardiomyocytes
Comparison
miR-375 inhibitor vs no miR-375 inhibitor in doxorubicin-treated models
Design
In vivo mouse and in vitro cell culture experimental study
Authors
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Hypothesis-generating for miR-375 inhibition in doxorubicin cardiotoxicity; leaves open clinical translation from animal data.
Does inhibition of miR-375 prevent oxidative damage and apoptosis in a mouse model of doxorubicin-induced cardiac toxicity?
Inhibition of miR-375 protects against doxorubicin-induced cardiac toxicity by reducing oxidative stress and apoptosis via the PDK1/AKT signaling pathway in preclinical models.
Zhang et al. (2020) studied Doxorubicin-induced cardiac toxicity. miR-375 inhibitor vs. Doxorubicin without miR-375 inhibitor was evaluated on Oxidative stress and cardiomyocyte apoptosis. Inhibition of miR-375 prevented doxorubicin-induced oxidative stress and cardiomyocyte apoptosis in vivo and in vitro through the PDK1/AKT signaling pathway.
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