Aberrant microRNAs are strongly associated with cardiac diseases. However, the regulation mechanism of MiR-181a in hypoxia-induced cardiomyocytes apoptosis and mitochondrial fragmentation have not been clarified. In the present study, we investigated the function of miR-181a in cardiomyocytes under hypoxic conditions. Cell viability, apoptosis, mitochondrial fragmentation, ROS level, activity of caspase 3 and 9, mitochondrial membrane potential, as well as primary antibodies Bcl-2, Bax, Drp1, MFN2, and Higd-1a levels in treated cells were tested. The results showed that overexpression of miR-181a led to an increase in apoptosis, ROS production, and mitochondrial membrane potential loss. Mechanistically, miR-181a promotes mitochondrial fission through targeting Higd-1a, and the effects of miR-181a could be rescued by Higd-1a. Collectively, our results are beneficial to understand the function of miR-181a in hypoxia-induced apoptosis and mitochondrial damage, which might become a novel direction for related diseases.
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Pang, Y., Lu, J., Lu, J., Pan, C., Wen, Z., Zhu, Z., Xiang, Q., Lin, H., Tang, M. (2024) MiR-181a promotes hypoxia-induced apoptosis and mitochondrial damage through regulating Higd-1a. Scientific Research Bulletin, 1(4), 35-44. https://doi.org/10.71052/srb2024/XBRB3109
