Abstract Fri139: Endotoxemia induces mitochondrial DNA (mtDNA) damage in mouse myocardium and cardiomyocytes

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Research shows LPS exposure increases mtDNA damage and inflammation in cardiomyocytes, suggesting potential therapeutic targets in sepsis.

Increased mtDNA damage observed in cardiac tissue from LPS-treated mice, indicating severe mitochondrial dysfunction.
Cardiomyocyte death correlated with elevated reactive oxygen species production after LPS exposure in cell models.
NRF2 and other key mitochondrial genes were downregulated, highlighting disrupted cellular mechanisms in sepsis.
Introducing healthy mitochondria reduced inflammation, suggesting a promising therapeutic strategy for cardiac complications.

Dubey et al. (2025) studied this question.

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Research shows LPS exposure increases mtDNA damage and inflammation in cardiomyocytes, suggesting potential therapeutic targets in sepsis.