Mitochondrial DNA, oxidants, and innate immunity.


Journal Article (Review)

Mitochondrial oxidant damage, including damage to mitochondrial DNA (mtDNA) is a feature of both severe microbial infections and inflammation arising from sterile (non-infectious) sources such as tissue trauma. Damaged mitochondria release intact or oxidized fragments of mtDNA into the cytoplasm, which represent oxidant injury, and the fragments promote a spontaneous innate immune response, exemplifying a modern frontier of immunological research. MtDNA and mitochondrial-derived oxidants are central factors in activating at least three innate immune pathways involving the TLR9 (Toll-like receptor 9), the NLRP3 (NACHT, LRR and PYD domains-containing protein-3) inflammasome, and the cGAS (cyclic AMP-GMP synthase) pathway. The events that allow mtDNA to escape from damaged mitochondria and from damaged cells are incompletely known, but the presence of cytoplasmic mtDNA and cell-free mtDNA as immune regulators are important for understanding the cell's capacity for protecting mitochondrial quality control (MQC) and cell viability during inflammatory states.

Full Text

Duke Authors

Cited Authors

  • Piantadosi, CA

Published Date

  • May 20, 2020

Published In

Volume / Issue

  • 152 /

Start / End Page

  • 455 - 461

PubMed ID

  • 31958498

Pubmed Central ID

  • 31958498

Electronic International Standard Serial Number (EISSN)

  • 1873-4596

Digital Object Identifier (DOI)

  • 10.1016/j.freeradbiomed.2020.01.013


  • eng

Conference Location

  • United States