Molecular and cellular consequences of mitochondrial DNA double-stranded breaks.
Chenxiao YuSamieh AsadianMarco TiganoPublished in: Human molecular genetics (2024)
Mitochondria are subcellular organelles essential for life. Beyond their role in producing energy, mitochondria govern various physiological mechanisms, encompassing energy generation, metabolic processes, apoptotic events, and immune responses. Mitochondria also contain genetic material that is susceptible to various forms of damage. Mitochondrial double-stranded breaks (DSB) are toxic lesions that the nucleus repairs promptly. Nevertheless, the significance of DSB repair in mammalian mitochondria is controversial. This review presents an updated view of the available research on the consequences of mitochondrial DNA DSB from the molecular to the cellular level. We discuss the crucial function of mitochondrial DNA damage in regulating processes such as senescence, integrated stress response, and innate immunity. Lastly, we discuss the potential role of mitochondrial DNA DSB in mediating the cellular consequences of ionizing radiations, the standard of care in treating solid tumors.
Keyphrases
- mitochondrial dna
- copy number
- cell death
- dna damage
- oxidative stress
- endoplasmic reticulum
- reactive oxygen species
- immune response
- genome wide
- healthcare
- binding protein
- dna methylation
- low dose
- palliative care
- quality improvement
- single molecule
- gene expression
- inflammatory response
- pain management
- risk assessment
- climate change