Impaired mitochondrial function induced by serum from septic shock patients is attenuated by inhibition of nitric oxide synthase and poly(ADP-ribose) synthase*

Boulos, Michael; Astiz, Mark E.; Barua, Rajat S.; Osman, Mohammed

doi:10.1097/01.ccm.0000050074.82486.b2

Cited by 115 publications

(58 citation statements)

References 29 publications

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“…87,88 Mitochondria are known to be a major intracellular source of ROS, 59 and incubation of cells in plasma taken from septic patients results in a marked depression of mitochondrial respiration with associated oxidative stress. 89 A relationship between sluggish microvascular flow and oxidative stress in AKI is now coming to the forefront. Oxidative stress in renal tubules has been coupled closely with sluggish blood flow in adjacent capillaries.…”

Section: Oxidative Stressmentioning

confidence: 99%

Sepsis-Associated AKI: Epithelial Cell Dysfunction

Emlet¹,

Shaw²,

Kellum³

2015

Seminars in Nephrology

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Section: Oxidative Stressmentioning

confidence: 99%

Sepsis-Associated AKI: Epithelial Cell Dysfunction

Emlet¹,

Shaw²,

Kellum³

2015

Seminars in Nephrology

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“…Moreover, mitochondrial dysfunction has been shown to be a key mechanism involved in organ failure, the hallmark of sepsis. One study demonstrated that serum from septic shock patients significantly impaired mitochondrial respiration in endothelial cells and decreased cellular ATP levels [9]. Previous studies have indicated that autophagy is associated with reduced intracellular ATP levels [10].…”

Section: Introductionmentioning

confidence: 98%

Infusion of a Glucose Solution Reduces Autophagy in the Liver after LPS-induced Systemic Inflammation

et al. 2011

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Autophagy is a natural process by which a cell maintains homeostasis, usually taking place unnoticed by adjacent cells. Glucose is involved in a negative feedback loop in autophagy. Autophagy is characterized by the induction and secretion of HMGB1, yet the nature of the inflammatory response during and the effect of glucose administration on autophagy are not well understood. Systemic inflammation was induced in experimental animals by LPS injection (7.5 mg/kg) followed by a continuous infusion of either 1%, 5%, or 25% glucose. Autophagy was visualized by immunohistochemistry 12 h after LPS injection. Likewise, protein levels of microtubule-associated protein light chain 3 (LC3)-II, autophagy-related protein 7 (Atg7), and high-mobility group box 1 (HMGB1) were assayed by western blot analysis. We found that autophagy increased in liver tissue in response to LPS-induced systemic inflammation. However, protein levels decreased in rats receiving LPS and a 5% glucose solution. Our results suggest that LPS-induced systemic inflammation increases autophagy in liver cells, potentially involving the upregulation of LC3-II, Atg7, and HMGB1. We also show that a 5% glucose infusion reduces autophagy. We propose that maintaining serum glucose levels with an adequate glucose dose improves systemic inflammation by reducing autophagy.

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“…In vitro, there is a significant correlation between SvO 2 and impairment of mitochondrial oxygen utilization. 42 The resultant tissue hypoxia can serve to further activate endothelial mediators, 22 causing loss of vascular integrity, 43 increased release of inflammatory cytokines 44 and procoagulants, 45 and reduced fibrinolysis. 46 …”

Section: Oxygen Transport and Utilizationmentioning

confidence: 99%