Septic cardiomyopathy is a significant morbid component of severe sepsis and septic shock. Further research into reducing cardiomyocyte damage via oxidative stress, reducing pro-inflammatory responses induced by TLR-4/NF-κβ signaling, decreasing mitochondrial dysfunction, and improving cellular respiration thereby decreasing apoptosis are examples of areas that may be future therapeutic targets.
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Balija et al. (2011) studied this question.
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