Publications by authors named "Christina M Heiestad"
Myocardial ischemia-reperfusion (IR) injury may result in cardiomyocyte dysfunction. Mitochondria play a critical role in cardiomyocyte recovery after IR injury. The mitochondrial uncoupling protein 3 (UCP3) has been proposed to reduce mitochondrial reactive oxygen species (ROS) production and to facilitate fatty acid oxidation.
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- The study investigates the role of extracellular histones as harmful molecules in acute myocardial infarction during ischaemia and reperfusion.
- Histones were found to be released early during reperfusion and were toxic to heart cells; however, using a histone-neutralizing compound significantly reduced heart tissue damage.
- The findings suggest that targeting extracellular histones could be a new strategy to protect heart cells from injury during myocardial infarction.
Background And Purpose: Cellular debris causes sterile inflammation after myocardial infarction. Mitochondria constitute about 30 percent of the human heart. Mitochondrial DNA (mtDNA) is a damage-associated-molecular-pattern that induce injurious sterile inflammation.
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