Why the study?
Although miR-124 was known to reduce oxidative stress and prevent apoptosis, its role in doxorubicin-induced cardiomyopathy was less known.
Does overexpression of miR-124 reduce oxidative stress and cell apoptosis in doxorubicin-treated heart tissues and primary cardiomyocytes?
Population
Doxorubicin-treated heart tissues and primary cardiomyocytes
Comparison
Overexpressing miR-124 vs inhibiting miR-124
Design
Preclinical laboratory study
Authors
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Should not yet change practice in doxorubicin cardiomyopathy; leaves open whether miR-124 targeting translates to humans.
Does overexpression of miR-124 reduce oxidative stress and cell apoptosis in doxorubicin-treated heart tissues and primary cardiomyocytes?
miR-124 attenuates doxorubicin-induced cardiac injury by inhibiting p66Shc-mediated oxidative stress, highlighting it as a potential therapeutic target for doxorubicin-related cardiomyopathy.
Liu et al. (2019) studied this question.
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