Abstract
Ischemia/reperfusion (I/R) in critical ill patients causes multiple organ dysfunction and eventually leads to mortality. Ischemia/reperfusion (I/R) injury is a common occurrence resulting from acute mesenteric ischemia, traumatic or septic shock, burns, and surgical procedures. Mitochondria are considered as cellular factory because of their ability to produce adenosine triphosphate (ATP). Recent studies suggest that mitochondrial dysfunction can promote inflammation, oxidative stress, and induce cell death, all of which can aggravate I/R injury. Mounting evidence showed that mitochondrial DNA (mtDNA) damage can induce mitochondrial dysfunction and induce I/R injury. Additionally, when mtDNA is released into the cytoplasm, extracellular milieu or circulation, it can activate multiple pattern-recognition receptors (PRRs) to trigger pro-inflammatory responses. We review the relationship between mtDNA damage and I/R, and speculate that mtDNA may be a potential target for I/R injury. Key words: Ischemia/reperfusion; Mitochondrial DNA; Inflammation
Published Version
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