Chronic kidney disease worsens sepsis and sepsis-induced acute kidney injury by releasing High Mobility Group Box Protein-1 - Wikidata - wikimedia - TriplyDB

Chronic kidney disease worsens sepsis and sepsis-induced acute kidney injury by releasing High Mobility Group Box Protein-1

Chronic kidney disease worsens sepsis and sepsis-induced acute kidney injury by releasing High Mobility Group Box Protein-1

http://www.wikidata.org/entity/Q36379017

about

The role of high mobility group box 1 (HMGB1) in the pathogenesis of kidney diseases Role of kidney injury in sepsis Toll-like receptor activation: from renal inflammation to fibrosis FGF23 signaling impairs neutrophil recruitment and host defense during CKD.Microparticles: markers and mediators of sepsis-induced microvascular dysfunction, immunosuppression, and AKI Update on sepsis-associated acute kidney injury: emerging targeted therapies Small Heat Shock Protein Beta-1 (HSPB1) Is Upregulated and Regulates Autophagy and Apoptosis of Renal Tubular Cells in Acute Kidney Injury Cellular and Molecular Mechanisms of AKI.Inflammation in AKI: Current Understanding, Key Questions, and Knowledge Gaps.Ultrasound Modulates the Splenic Neuroimmune Axis in Attenuating AKI.Reduction of Tubular Flow Rate as a Mechanism of Oliguria in the Early Phase of Endotoxemia Revealed by Intravital Imaging Hemostasis biomarkers and risk of sepsis: the REGARDS cohort.Abandon the mouse research ship? Not just yet!HMGB1 in health and disease.Impact of non-dialysis chronic kidney disease on survival in patients with septic shock.How can antibiotics worsen acute kidney injury but improve survival in experimental sepsis?High-dose ascorbate with low-dose amphotericin B attenuates severity of disease in a model of the reappearance of candidemia during sepsis in the mouse.TLR4 mutant mice are protected from renal fibrosis and chronic kidney disease progression High-mobility group box 1 inhibits HCO(3)(-) absorption in medullary thick ascending limb through a basolateral receptor for advanced glycation end products pathway Development of intestinal ischemia/reperfusion-induced acute kidney injury in rats with or without chronic kidney disease: Cytokine/chemokine response and effect of α-melanocyte-stimulating hormone.HMGB1 mediates anemia of inflammation in murine sepsis survivors.A two-hit mechanism for sepsis-induced impairment of renal tubule function Could Biomarkers Direct Therapy for the Septic Patient?Bridging translation for acute kidney injury with better preclinical modeling of human disease AUF1-RGG peptides up-regulate the VEGF antagonist, soluble VEGF receptor-1 (sFlt-1).Lumen LPS inhibits HCO3(-) absorption in the medullary thick ascending limb through TLR4-PI3K-Akt-mTOR-dependent inhibition of basolateral Na+/H+ exchange Future potential biomarkers for postinterventional restenosis and accelerated atherosclerosis.Beyond tissue injury-damage-associated molecular patterns, toll-like receptors, and inflammasomes also drive regeneration and fibrosis.Clinical study of blood purification therapy in critical care in Japan: results from the survey research of the Japan Society for Blood Purification in Critical Care in 2013.The in vivo evidence for regulated necrosis.Cumulative Fluid Balance and Mortality in Septic Patients With or Without Acute Kidney Injury and Chronic Kidney Disease.High-mobility group box 1 inhibits HCO3- absorption in the medullary thick ascending limb through RAGE-Rho-ROCK-mediated inhibition of basolateral Na+/H+ exchange.IκB Kinase Inhibitor Attenuates Sepsis-Induced Cardiac Dysfunction in CKD.HMGB1 redox during sepsis Blood purification treatment initiated at the time of sepsis diagnosis effectively attenuates serum HMGB1 upregulation and improves patient prognosis.HMGB1, TGF-β and NF-κB are associated with chronic allograft nephropathy.Macrophage Uptake of Necrotic Cell DNA Activates the AIM2 Inflammasome to Regulate a Proinflammatory Phenotype in CKD.AKI on CKD: heightened injury, suppressed repair, and the underlying mechanisms.Longitudinal changes in MRI markers in a reversible unilateral ureteral obstruction mouse model: preliminary experience.Protection of resveratrol on acute kidney injury in septic rats.

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Chronic kidney disease worsens sepsis and sepsis-induced acute kidney injury by releasing High Mobility Group Box Protein-1

http://www.wikidata.org/entity/Q36379017

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Kidney International

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Asada Leelahavanichkul

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Hua Zhou

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Jürgen Schnermann

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Richard Chen

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Robert A Star

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Takayuki Tsuji

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Xuzhen Hu

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Yuning Huang

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P2860

Structural basis for the proinflammatory cytokine activity of high mobility group box 1

Vascular endothelial growth factor is an important determinant of sepsis morbidity and mortality

The biology of VEGF and its receptors

Epidemiology of severe sepsis in the United States: analysis of incidence, outcome, and associated costs of care

Release of chromatin protein HMGB1 by necrotic cells triggers inflammation

HMG-1 as a late mediator of endotoxin lethality in mice

A cardiovascular drug rescues mice from lethal sepsis by selectively attenuating a late-acting proinflammatory mediator, high mobility group box 1

High mobility group 1 protein (HMG-1) stimulates proinflammatory cytokine synthesis in human monocytes

The epidemiology of sepsis in the United States from 1979 through 2000

The pathophysiology and treatment of sepsis

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scholarly article

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10.1038/KI.2011.261

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11

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80

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Jeffrey B. Kopp

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51563175

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