Molecular and cellular consequences of mitochondrial DNA double-stranded breaks

Author:

Yu Chenxiao12,Asadian Samieh3,Tigano Marco1ORCID

Affiliation:

1. Thomas Jefferson University Department of Pathology and Genomic Medicine, , 1020 Locust Street, Philadelphia 19107, United States

2. The Second Affiliated Hospital of Soochow University Department of Radiotherapy and Oncology, , 199 Renai Road, Suzhou 215123, China

3. Tehran University of Medical Sciences , Pour Sina St, Tehran 1416634793, Iran

Abstract

Abstract 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.

Funder

National Institutes of Health

Publisher

Oxford University Press (OUP)

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