# Advances in Elucidating the Mitochondrial DNA Mechanisms Underlying Ozone-Induced Inflammation

## TL;DR

This paper reviews how mitochondrial DNA might be involved in inflammation caused by ozone exposure.

## Contribution

The paper provides a review of how mitochondrial DNA functions as a mediator in ozone-induced inflammation.

## Key findings

- Ozone exposure may lead to mitochondrial dysfunction and mtDNA release.
- mtDNA could act as a damage-related molecular pattern triggering inflammation.
- The paper reviews mechanisms linking ozone exposure to inflammatory responses.

## Abstract

Ground-level ozone is widely acknowledged as one of the primary air pollutants, capable of inducing adverse health effects across multiple human systems, including asthma, cardiovascular events, and central nervous system dysfunction. Epidemiological and toxicological studies indicate that the onset of related systemic diseases is often attributed to ozone-mediated inflammatory responses. However, since O3 itself lacks antigenic properties to trigger innate immune responses, an intermediary substance induced by ozone exposure likely activates subsequent inflammatory pathways. Multiple ozone exposure studies have identified mitochondrial DNA (mtDNA) as a potential biomarker released during ozone-induced mitochondrial dysfunction. mtDNA may serve as a damage-related molecular pattern that activates innate immune responses, potentially acting as a crucial link between ozone and inflammatory reactions. This review therefore examines the structure and function of mitochondrial DNA, along with potential mediating mechanisms underlying inflammation associated with ozone exposure.