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Interactions between cardiac miRNAs and ROS have been demonstrated across various cardiovascular events, including DbCM, atherosclerosis and MI in animal models, where they drive necrosis, fibrosis, apoptosis, hypertrophy, and proliferation, in VSMCs, cardiomyocytes, endothelial cells, and cardiac fibroblasts [136]

In contrast, under mitochondrial mistranslation stress, our screen identified the v-ATPase as the sole extra-mitochondrial effector mitigating mitochondrial dysfunction

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