Deficient mitochondrial biogenesis in critical illness: cause, effect, or epiphenomenon?
- PMID: 17764588
- PMCID: PMC2206497
- DOI: 10.1186/cc6098
Deficient mitochondrial biogenesis in critical illness: cause, effect, or epiphenomenon?
Abstract
Recent studies indicate that mitochondrial dysfunction plays a role in the pathogenesis of a number of disease states. The importance of these organelles in shock and multiple organ dysfunction is of particular interest to those caring for the critically ill. Mitochondria have their own unique DNA (mtDNA) that encodes 13 essential subunits of electron transport chain enzymes, two ribosomal RNAs and 22 transfer RNAs. Importantly, mtDNA is especially susceptible to deletions, rearrangements and mutations because it is not bound by histones and lacks the extensive repair machinery present in the nucleus. The study by Côté et al. in this issue of Critical Care examines changes in mtDNA in critically ill patients. The results support further investigation into the role of mtDNA in the critically ill.
Comment on
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Longitudinal increases in mitochondrial DNA levels in blood cells are associated with survival in critically ill patients.Crit Care. 2007;11(4):R88. doi: 10.1186/cc6096. Crit Care. 2007. PMID: 17697385 Free PMC article.
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