Key result
LPS-induced endotoxemia increases cardiomyocyte death and inflammation driven by mitochondrial ROS and mtDNA damage.
Why the study?
Does LPS-induced endotoxemia cause mitochondrial DNA damage and cardiomyocyte death, and can exogenous healthy mitochondria mitigate these effects in preclinical models?
Population
Adult C57BL/6 mice, human Ac16 ventricular cardiomyocytes, mouse neonatal cardiomyocytes, and HL-1 cells
Comparison
Lipopolysaccharide 2mg/kg intraperitoneally or… vs Untreated controls
Design
Preclinical
Follow-up
24 hours (in vivo), 24 or 72 hours (in vitro)
Authors
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Endotoxemia induces mitochondrial DNA damage and cardiomyocyte death, which may be mitigated by the exogenous delivery of healthy mitochondria, suggesting a novel therapeutic target for sepsis-induced cardiovascular complications.
Does LPS-induced endotoxemia cause mitochondrial DNA damage and cardiomyocyte death, and can exogenous healthy mitochondria mitigate these effects in preclinical models?
Endotoxemia induces mitochondrial DNA damage and cardiomyocyte death, which may be mitigated by the exogenous delivery of healthy mitochondria, suggesting a novel therapeutic target for sepsis-induced cardiovascular complications.
Dubey et al. (2025) studied Sepsis-induced cardiovascular dysfunction. Lipopolysaccharide (LPS) vs. Control / untreated cells was evaluated on mtDNA damage, inflammation, mitoROS production, and cell death. LPS-induced endotoxemia increased mitochondrial ROS production, mtDNA damage, inflammation, and cardiomyocyte death in mice and cell lines.
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