Key result
Cardiac-specific overexpression of miR-199a-3p relieved doxorubicin-induced cardiac senescence and inhibited the generation of senescence-associated secretory phenotype via GATA4 modulation.
Why the study?
Clinical use of the anticancer agent doxorubicin is hampered by cardiotoxicity, prompting investigation into the cardioprotective potential of miR-199a-3p.
Does miR-199a-3p overexpression prevent cardiac senescence in cardiomyocytes exposed to doxorubicin?
Population
Cardiomyocytes exposed to doxorubicin
Comparison
Cardiac-specific overexpression of miR-199a-3p vs controls
Authors
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May attenuate Dox-induced senescence in models; leaves open clinical translation for cardioprotection.
Does miR-199a-3p overexpression prevent cardiac senescence in cardiomyocytes exposed to doxorubicin?
Overexpression of miR-199a-3p may offer a therapeutic strategy to prevent doxorubicin-induced cardiotoxicity by reducing cardiac senescence and its spread.
Xia et al. (2021) studied Doxorubicin-related cardiotoxicity. miR-199a-3p overexpression was evaluated on Cardiac senescence and SASP generation. Cardiac-specific overexpression of miR-199a-3p relieved doxorubicin-induced cardiac senescence and inhibited the generation of senescence-associated secretory phenotype via GATA4 modulation.
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