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Molecular and Cellular Consequences of Mitochondrial Dna Double-Stranded Breaks Publisher Pubmed



Yu C1, 2 ; Asadian S3 ; Tigano M1
Authors
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Authors Affiliations
  1. 1. Department of Pathology and Genomic Medicine, Thomas Jefferson University, 1020 Locust Street, Philadelphia, 19107, United States
  2. 2. Department of Radiotherapy and Oncology, The Second Affiliated Hospital of Soochow University, 199 Renai Road, Suzhou, 215123, China
  3. 3. Tehran University of Medical Sciences, Pour Sina St, Tehran, 1416634793, Iran

Source: Human Molecular Genetics Published:2024


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. © 2024 The Author(s). Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.
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