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suck abstract from ncbi


10.1097/SHK.0000000000000463

http://scihub22266oqcxt.onion/10.1097/SHK.0000000000000463
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C4755359!4755359!26871665
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suck abstract from ncbi

pmid26871665      Shock 2016 ; 45 (3): 271-81
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  • Mitochondrial Function in Sepsis #MMPMID26871665
  • Arulkumaran N; Deutschman CS; Pinsky MR; Zuckerbraun B; Schumacker PT; Gomez H; Gomez A; Murray P; Kellum JA
  • Shock 2016[Mar]; 45 (3): 271-81 PMID26871665show ga
  • Mitochondria are an essential part of the cellular infrastructure, being the primary site for high energy adenosine triphosphate (ATP) production through oxidative phosphorylation. Clearly, in severe systemic inflammatory states, like sepsis, cellular metabolism is usually altered and end organ dysfunction not only common but predictive of long term morbidity and mortality. Clearly, interest is mitochondrial function both as a target for intracellular injury and response to extrinsic stress have been a major focus of basic science and clinical research into the pathophysiology of acute illness. However, mitochondria have multiple metabolic and signaling functions that may be central in both the expression of sepsis and its ultimate outcome. In this review, the authors address five primary questions centered on the role of mitochondria in sepsis. This review should be used as both a summary source in placing mitochondrial physiology within the context of acute illness and as a focal point for addressing new research into diagnostic and treatment opportunities these insights provide.
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