Key result
miR-143 increases oxidative stress and myocardial apoptosis in murine doxorubicin cardiotoxicity by inhibiting AKT.
Why the study?
Although miR-143 is expressed in the myocardium and affects cardiac function, its effects and molecular mechanisms on oxidative stress and myocardial cell apoptosis in doxorubicin-induced cardiac toxicity were unclear.
Does miR-143 inhibition reduce oxidative stress and myocardial cell apoptosis in a mouse model of doxorubicin-induced cardiac toxicity?
Population
Mouse model of doxorubicin-induced cardiac toxicity
Comparison
miR-143 antagonist, miR-143 agomir, and AKT inhibitor MK2206
Design
Animal experimental study
Authors
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miR-143 modulation may attenuate doxorubicin cardiotoxicity in mice; leaves open translation to human cardioprotection.
Does miR-143 inhibition reduce oxidative stress and myocardial cell apoptosis in a mouse model of doxorubicin-induced cardiac toxicity?
Inhibition of miR-143 may protect against doxorubicin-induced cardiac toxicity by reducing oxidative stress and apoptosis via AKT pathway activation.
Li et al. (2020) studied Doxorubicin-induced cardiac toxicity. miR-143 antagomir was evaluated on Oxidative stress and myocardial cell apoptosis. In a mouse model of doxorubicin-induced cardiac toxicity, miR-143 increased oxidative stress and myocardial cell apoptosis following doxorubicin treatment by inhibiting AKT.
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