tailieunhanh - Báo cáo y học: "Deficient mitochondrial biogenesis in critical illness: cause, effect, or epiphenomeno"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Critical Care giúp cho các bạn có thêm kiến thức về ngành y học đề tài: Deficient mitochondrial biogenesis in critical illness: cause, effect, or epiphenomenon? | Available online http content 11 4 158 Commentary Deficient mitochondrial biogenesis in critical illness cause effect or epiphenomenon Richard J Levy1 and Clifford S Deutschman2 1 Maria Fareri Children s Hospital of Westchester Medical Center New York Medical College Valhalla New York USA 2Department of Anesthesiology and Critical Care and the Stavropoulos Sepsis Research Program University of Pennsylvania School of Medicine Philadelphia Pennsylvania USA Corresponding author Clifford S Deutschman deutschcl@ Published 24 August 2007 This article is online at http content 11 4 158 2007 BioMed Central Ltd Critical Care 2007 11 158 doi cc6098 See related research by Côté et al. http content 11 4 R88 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. The role of mitochondria in systemic disease has been underappreciated and in this issue of Critical Care Côté et al. 1 examine changes in mitochondrial DNA mtDNA in critically ill patients. However recent evidence has demonstrated impaired oxidative phosphorylation and defective mitochondrial homeostasis in a number of disorders 2 3 . Although the concept of mitochondrial dysfunction and bioenergetic failure during .

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