MIEF2, also known as mitochondrial elongation factor 2 or MiD49, is a key regulator of mitochondrial fission. It is a mitochondrial outer membrane protein that functions in modulating mitochondrial dynamics, which is crucial for many cellular processes such as apoptosis, mitophagy, and metabolic regulation [2,3,6,7,8]. It is associated with pathways like ROS/AKT/mTOR signaling, and its regulation is also influenced by factors like Foxo3a [1,5].

In ovarian cancer, MIEF2 promotes lipid synthesis by up-regulating SREBP1 and SREBP2 and their target genes, driving cancer progression through the ROS/AKT/mTOR pathway [1]. In the same cancer type, its over-expression promotes tumor growth and metastasis by reprogramming glucose metabolism from oxidative phosphorylation to glycolysis [2]. In colorectal cancer, loss of MIEF2, as identified by CRISPR-based knockout screening, enhances oxaliplatin resistance by inhibiting the mitochondrial apoptosis pathway [4]. In cardiomyocytes, knockdown of MIEF2 reduces doxorubicin-induced mitochondrial fission, apoptosis, and cardiotoxicity, with Foxo3a suppressing MIEF2 expression [5].

In conclusion, MIEF2 plays a significant role in multiple biological processes related to mitochondrial function and metabolism. Its dysregulation is associated with diseases such as ovarian cancer, colorectal cancer, and doxorubicin-induced cardiotoxicity. Studies using gene knockout or knockdown models have been instrumental in revealing its functions in these disease conditions, providing potential therapeutic targets for treatment [1,2,4,5].