TLR4 activation mediates kidney ischemia/reperfusion injury.

By Hui-ling Wu, G. Chen, K. Wyburn, Jianlin Yin, P. Bertolino, J. Eris, S. Alexander, Alexandra F. Sharland, S. Chadban. Journal of Clinical Investigation, 2007

870 citations recorded by the source corpus.

Subfields: Clinical Biochemistry, Immunology

View Paper: https://www.semanticscholar.org/paper/de414429599a411c0a6989b0251b17e50522ce81

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Clinical Biochemistry

1. R. Dhupar
2. Jon S. Cardinal
3. J. Klune
4. A. Tsung
5. Timothy R. Billiar

In Immunology

1. S. Iyer
2. R. Flavell
3. S. Eisenbarth
4. F. Sutterwala
5. Shizuo Akira
6. Alexander Y. Rudensky
7. R. Medzhitov

Citations in the corpus

• Delayed Graft Function in the Kidney Transplant (2011, background): “In response to ischemic kidney injury, however, tubular epithelial cells and mesangial cells express TLRs without direct contribution from the complement system (111,112).”
• Ischemia and reperfusion—from mechanism to translation (2011, background): “Mice with a genetic deletion of Tlr4 are protected from kidney ischemia, and experiments using bone-marrow chimeric mice suggest that kidney-intrinsic Tlr4 signaling has the predominant role in mediating kidney injur”
• Pathophysiology of Acute Kidney Injury (2012, neutral): “Mice typically manifest significant injury with shorter ischemic times in the range of 25 minutes (609) with some reports of significant necrosis resulting from an injury in as little as 17 minutes (266).”
• Necrotic cells trigger a sterile inflammatory response through the Nlrp3 inflammasome (2009, result): “S7 A and B), consistent with previous findings (28).”
• Hyaluronan as an Immune Regulator in Human Diseases (2011, neutral): “Recently, it was shown that TLR4 signaling through the MyD88-dependent pathway was required for the full development of kidney ischemia/reperfusion injury, as both TLR4- and MyD88-deficient mice were protected against kidney dysfunction, tubular damage, neutrophil and macrophage accumulation, and ex”
• HMGB1: Endogenous Danger Signaling (2008, background): “While the significant body of literature described above elucidates the role of HMGB1 in hepatic IRI, similar work in other organ systems including the heart (120,121), kidney (122), and brain (123–125) has provided confirmatory evidence that HMGB1 is involved in the initiation of the inflammatory r”