TLR4 signaling mediates inflammation and tissue injury in nephrotoxicity. - Wikidata - wikimedia - TriplyDB

TLR4 signaling mediates inflammation and tissue injury in nephrotoxicity.

TLR4 signaling mediates inflammation and tissue injury in nephrotoxicity.

http://www.wikidata.org/entity/Q36662114

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New Therapeutic Concept of NAD Redox Balance for Cisplatin Nephrotoxicity Guidance cue netrin-1 and the regulation of inflammation in acute and chronic kidney disease Trauma equals danger--damage control by the immune system Mechanisms of Cisplatin nephrotoxicity How the Innate Immune System Senses Trouble and Causes Trouble Mining kidney toxicogenomic data by using gene co-expression modules Endotoxin uptake by S1 proximal tubular segment causes oxidative stress in the downstream S2 segment.Renal dendritic cells ameliorate nephrotoxic acute kidney injury The regulation of inflammatory mediators in acute kidney injury via exogenous mesenchymal stem cells.TLR4 activation promotes podocyte injury and interstitial fibrosis in diabetic nephropathy.Acute kidney injury: a springboard for progression in chronic kidney disease Toll-like receptors in kidney disease.Pathophysiology of cisplatin-induced acute kidney injury.Cellular responses to Cisplatin-induced DNA damage.Toll-like receptor 4 in bone marrow-derived cells contributes to the progression of diabetic retinopathy.Renal effects of treatment with a TLR4 inhibitor in conscious septic sheep.Toll-like receptor tolerance as a mechanism for neuroprotection.p53 target Siva regulates apoptosis in ischemic kidneys.Lipopolysaccharide signaling without a nucleus: kinase cascades stimulate platelet shedding of proinflammatory IL-1β-rich microparticles.TWEAK-Fn14 as a mediator of acute kidney injury.Pharmacological and molecular effects of platinum(II) complexes involving 7-azaindole derivatives.Tissue-type plasminogen activator (tPA) promotes M1 macrophage survival through p90 ribosomal S6 kinase (RSK) and p38 mitogen-activated protein kinase (MAPK) pathway Endogenous IL-10 attenuates cisplatin nephrotoxicity: role of dendritic cells Cisplatin induces primary necrosis through poly(ADP-ribose) polymerase 1 activation in kidney proximal tubular cells Computational approaches for translational clinical research in disease progression.Poly(ADP-ribose) polymerase-1 is a key mediator of cisplatin-induced kidney inflammation and injury.Inhibition of PKCδ reduces cisplatin-induced nephrotoxicity without blocking chemotherapeutic efficacy in mouse models of cancer Basolateral LPS inhibits NHE3 and HCOFormula absorption through TLR4/MyD88-dependent ERK activation in medullary thick ascending limb Mitochondrial-targeted antioxidants represent a promising approach for prevention of cisplatin-induced nephropathy Diagnostic value of urine sTREM-1 for sepsis and relevant acute kidney injuries: a prospective study.Dendritic Cell Protection from Cisplatin Nephrotoxicity Is Independent of Neutrophils.Toll-like receptor 2 is required for LPS-induced Toll-like receptor 4 signaling and inhibition of ion transport in renal thick ascending limb.Tissue plasminogen activator activates NF-κB through a pathway involving annexin A2/CD11b and integrin-linked kinase.TLR4 mutant mice are protected from renal fibrosis and chronic kidney disease progression Role of Toll-like receptors in diabetic renal lesions in a miniature pig model.Puerarin attenuates cisplatin-induced rat nephrotoxicity: The involvement of TLR4/NF-κB signaling pathway Precocious obesity predisposes the development of more severe cisplatin-induced acute kidney injury in young adult mice.TNF-α mediates increased susceptibility to ischemic AKI in diabetes.No longer an innocent bystander: epithelial toll-like receptor signaling in the development of mucosal inflammation A two-hit mechanism for sepsis-induced impairment of renal tubule function

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P2860

TLR4 signaling mediates inflammation and tissue injury in nephrotoxicity.

http://www.wikidata.org/entity/Q36662114

description

2008 nî lūn-bûn

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name

TLR4 signaling mediates inflammation and tissue injury in nephrotoxicity.

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TLR4 signaling mediates inflammation and tissue injury in nephrotoxicity.

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TLR4 signaling mediates inflammation and tissue injury in nephrotoxicity.

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TLR4 signaling mediates inflammation and tissue injury in nephrotoxicity.

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TLR4 signaling mediates inflammation and tissue injury in nephrotoxicity.

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TLR4 signaling mediates inflammation and tissue injury in nephrotoxicity.

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Journal of the American Society of Nephrology

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TLR4 signaling mediates inflammation and tissue injury in nephrotoxicity.

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P2093

Binzhi Zhang

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Ganesan Ramesh

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Satoshi Uematsu

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W Brian Reeves

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P2860

Defective LPS Signaling in C3H/HeJ and C57BL/10ScCr Mice: Mutations in Tlr4 Gene

Induction of apoptosis by ASK1, a mammalian MAPKKK that activates SAPK/JNK and p38 signaling pathways

Signaling danger: toll-like receptors and their potential roles in kidney disease

Cutting edge: Toll-like receptor 4 (TLR4)-deficient mice are hyporesponsive to lipopolysaccharide: evidence for TLR4 as the Lps gene product

Impaired IL-18 processing protects caspase-1-deficient mice from ischemic acute renal failure

Neutralization of Gro alpha and macrophage inflammatory protein-2 attenuates renal ischemia/reperfusion injury

Cutting edge: heat shock protein 60 is a putative endogenous ligand of the toll-like receptor-4 complex

DAMPs, PAMPs and alarmins: all we need to know about danger

Tamm-Horsfall glycoprotein links innate immune cell activation with adaptive immunity via a Toll-like receptor-4-dependent mechanism.

Renal-associated TLR2 mediates ischemia/reperfusion injury in the kidney

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923-932

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10.1681/ASN.2007090982

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5

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18256356

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Toll-like receptor

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