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Damaged mitochondria result in electron leakage, produce increased ROS, and release cytochrome C leading to activation of caspase-3, caspase-9, and other pro-apoptotic factors ultimately leading to cell death (Brustovetsky et al., 2008

Because there is an increase in ROS, a feedback loop exists where the increase in ROS causes an increase in production of reduced glutathione to combat the increased ROS production

Similarly, the role of Fra2/BolA2 in human cells is largely unknown, although the mitochondrially targeted BolA3 is involved in FeS cluster acquisition and/or maintenance for some mitochondrial FeS enzymes, especially lipoate synthase (

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Additionally, YTHDF2 degrades EGR1 mRNA via m 6 A modification, hence disrupting the transcription of p21 cip1/waf1 and increasing the expression of CDK2-cyclinE1, which promotes the proliferation of MM cells [245]