What does this research mean for the field?

Overexpression of miR-210 significantly reduces apoptotic cell death in AC-16 cardiomyocytes subjected to doxorubicin treatment. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

This research investigates the cardioprotective role of miR-210 against doxorubicin-induced cardiotoxicity.

January 10, 2026Cardio-Oncology0 citationsOpen Access

Cardiomyocyte overexpression of microRNA-210 mitigates apoptotic cell death induced by doxorubicin

JGJohan GuthormsenNorwegian University of Science and Technology MØMikal Solstad ØiaasNorwegian University of Science and Technology MAMido Magdi AllamNorwegian University of Science and Technology

Key Result

Overexpression of miR-210 significantly reduced apoptotic cell death in AC-16 cardiomyocytes subjected to doxorubicin treatment, compared to downregulation.

Key Points

This research investigates the cardioprotective role of miR-210 against doxorubicin-induced cardiotoxicity.
Used AC-16 cardiomyocytes for experiments.
Upregulated or downregulated miR-210 using transfection vectors.
Exposed cells to doxorubicin for 24 hours.
Measured cell death through lactate dehydrogenase release assay.
Assessed apoptotic cell death by caspase-3 activity assay.
Overexpression of miR-210 significantly reduced cell death.
Decreased apoptotic cell death was observed with miR-210 overexpression.
Downregulation of miR-210 resulted in increased apoptotic cell death.
Increased phosphorylation of GSK-3β and Akt was noted in the overexpression group.

Structured PICO

Does miR-210 overexpression prevent doxorubicin-induced apoptotic cell death in human AC-16 cardiomyocytes?

Population

Human AC-16 cardiomyocytes (n=16 cell culture plates, 4 per group) cultured in DEM/F12.

Intervention

Upregulation (overexpression) or downregulation (knockdown) of miR-210 using transient expression or decoy/inhibitory transfection vectors, followed by 5 µM doxorubicin treatment for 24 hours.

Comparator

Empty vector (EV) transfection followed by 5 µM doxorubicin or vehicle (sterile water) treatment for 24 hours.

Outcome

Cell death measured by lactate dehydrogenase (LDH) release assay and apoptotic cell death measured by caspase-3 activity assay at 24 hours.surrogate

Overexpression of miR-210 mitigates doxorubicin-induced cardiomyocyte apoptosis in vitro by modulating the Akt-GSK-3β signaling pathway, suggesting a potential therapeutic target for chemotherapy-induced cardiotoxicity.

Main Result

Absolute Event Rate: 0% vs 0%

Abstract

Advancements in cancer diagnostics and treatments have significantly increased patient survival rates. However, these advancements are often accompanied by treatment-induced health issues. Among these, chemotherapy-induced cardiac damage is particularly concerning, with doxorubicin being notably cardiotoxic. Despite extensive research, effective strategies to protect the heart from doxorubicin-induced cardiotoxicity remain elusive. This study aims to investigate whether miR-210, which has previously shown cardioprotective properties against ischemic heart disease, can offer protection against doxorubicin-induced cardiotoxicity. miR-210 was upregulated or downregulated in AC-16 cardiomyocytes using transient expression or decoy/inhibitory transfection vectors before being subjected to 5 µM doxorubicin treatment for 24 h. Cell death was determined using a lactate dehydrogenase release assay. Apoptotic cell death was determined by a caspase-3 activity assay, and the Akt-GSK-3β signaling pathway was explored using a sandwich enzyme-linked immunosorbent assay (ELISA) approach. Overexpression of miR-210 in AC-16 cardiomyocytes exposed to 24 h of doxorubicin treatment caused a significant reduction in cell death and a significant reduction in apoptotic cell death, measured by caspase-3 activity. Downregulation of miR-210 in AC-16 cardiomyocytes exposed to the same conditions resulted in a significant increase in apoptotic cell death. An increase in phosphorylation of GSK-3β at the inhibitory p-Ser9 site and the Akt activating site p-Ser473 was observed in the miR-210 overexpression group, while a decrease in p-Ser473 Akt but no difference in p-Ser9 GSK-3β was observed in the miR-210-downregulated group. miR-210 exerts cardioprotective effects in AC-16 cardiomyocytes exposed to 24 h of doxorubicin treatment by reducing cell death and inhibiting caspase-3 dependent apoptosis through modulation of the Akt-GSK-3β signaling pathway. This study suggests a novel role for miR-210 in mitigating DOX-induced cardiomyocyte death, potentially laying the foundation for new treatment strategies.

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