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Updated: Aug 15, 2025
Measuring Carbon Content in Airway Macrophages Exposed to Carbon-Containing Particulate Matters
Published on: July 12, 2024
Cell-free circulating mitochondrial DNA: An emerging biomarker for airborne particulate matter associated with
Afreen Rehman1, Roshani Kumari1, Arunika Kamthan1
1Department of Molecular Biology, ICMR-National Institute for Research in Environmental Health, Bhopal, India.
Abstract:
The association of airborne particulate matter exposure with the deteriorating function of the cardiovascular system is fundamentally driven by the impairment of mitochondrial-nuclear crosstalk orchestrated by aberrant redox signaling. The loss of delicate balance in retrograde communication from mitochondria to the nucleus often culminates in the methylation of the newly synthesized strand of mitochondrial DNA (mtDNA) through DNA methyl transferases. In highly metabolic active tissues such as the heart, mtDNA's methylation state alteration impacts mitochondrial bioenergetics. It affects transcriptional regulatory processes involved in biogenesis, fission, and fusion, often accompanied by the integrated stress response. Previous studies have demonstrated a paradoxical role of mtDNA methylation in cardiovascular pathologies linked to air pollution. A pronounced alteration in mtDNA methylation contributes to systemic inflammation, an etiological determinant for several co-morbidities, including vascular endothelial dysfunction and myocardial injury. In the current article, we evaluate the state of evidence and examine the considerable promise of using cell-free circulating methylated mtDNA as a predictive biomarker to reduce the more significant burden of ambient air pollution on cardiovascular diseases.
Insights
Airborne particulate matter harms cardiovascular health by disrupting mitochondrial DNA (mtDNA) methylation, affecting heart function. Cell-free methylated mtDNA shows promise as a biomarker for air pollution-related cardiovascular diseases.
Area of Science:
- Environmental Health
- Cardiovascular Biology
- Mitochondrial Medicine
Background:
- Airborne particulate matter exposure impairs cardiovascular function via disrupted mitochondrial-nuclear crosstalk and aberrant redox signaling.
- Mitochondrial DNA (mtDNA) methylation alterations, driven by DNA methyl transferases, impact cardiac bioenergetics and transcriptional regulation.
- mtDNA methylation plays a paradoxical role in cardiovascular pathologies, contributing to inflammation, vascular dysfunction, and myocardial injury.
Purpose of the Study:
- To evaluate the evidence linking airborne particulate matter exposure to cardiovascular dysfunction through mtDNA methylation.
- To examine the potential of cell-free circulating methylated mtDNA as a predictive biomarker for air pollution-related cardiovascular diseases.
Main Methods:
- Review of existing scientific literature on particulate matter, mtDNA methylation, and cardiovascular diseases.
- Analysis of the mechanisms underlying mtDNA methylation alterations in response to environmental exposures.
- Assessment of the utility of cell-free circulating methylated mtDNA as a diagnostic or prognostic tool.
Main Results:
- Aberrant redox signaling and impaired mitochondrial-nuclear crosstalk are key mechanisms linking particulate matter to cardiovascular issues.
- mtDNA methylation changes affect mitochondrial function, gene expression, and integrated stress response in the heart.
- Altered mtDNA methylation is associated with systemic inflammation and contributes to vascular endothelial dysfunction and myocardial injury.
Conclusions:
- Cell-free circulating methylated mtDNA presents a promising biomarker for predicting cardiovascular risks associated with ambient air pollution.
- Understanding mtDNA methylation's role is crucial for developing strategies to mitigate the cardiovascular burden of air pollution.
