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REVIEW article

Front. Cell. Infect. Microbiol.
Sec. Bacteria and Host
Volume 14 - 2024 | doi: 10.3389/fcimb.2024.1529441
This article is part of the Research Topic Bacteria-Host Interactions: From Infection to Carcinogenesis View all 6 articles

Decoding mitochondria DNA damage and repair associated with H. pylori infection

Provisionally accepted
Dawit Kidane Dawit Kidane *Aashirwad Shahi Aashirwad Shahi
  • College of Medicine, Howard University, Washington DC, United States

The final, formatted version of the article will be published soon.

    Mitochondrial genomic stability is critical for preventing various human inflammatory diseases. Bacterial infection significantly increases oxidative stress, driving mitochondrial genomic instability and initiating inflammatory human disease. Oxidative DNA base damage is predominantly repaired by base excision repair (BER) in the nucleus (nBER) as well as in the mitochondria (mtBER). In this review, we summarize the molecular mechanisms of spontaneous and H. pylori infection associated oxidative mtDNA damage, mtDNA replication stress and its impact on innate immune signaling.Additionally, we discuss how mutations located on mitochondria targeting sequence (MTS) of BER genes may contribute to mtDNA genome instability and innate immune signaling activation. Overall, the review summarizes evidence to understand the dynamics of mitochondria genome and the impact of mtBER in innate immune response during H. pylori associated pathological outcomes.

    Keywords: Mitochondria DNA damage, repair, H. pylori and innate immune signaling Font: (Default) Arial, 12 pt, Base excision DNA repair, cGAS-STING

    Received: 16 Nov 2024; Accepted: 19 Dec 2024.

    Copyright: © 2024 Kidane and Shahi. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Dawit Kidane, College of Medicine, Howard University, Washington DC, United States

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.