Acute kidney injury: a conspiracy of Toll-like receptor 4 on endothelia, leukocytes, and tubules.
Ischemic acute kidney injury (AKI) contributes to considerable morbidity and mortality in hospitalized patients and can contribute to rejection during kidney transplantation. Maladaptive immune responses can exacerbate injury, and targeting these responses holds promise as therapy for AKI. In the last decade, a number of molecules and receptors were identified in the innate immune response to ischemia-reperfusion injury. This review primarily focuses on one pathway that leads to maladaptive inflammation: toll-like receptor 4 (TLR4) and one of its ligands, high mobility group box protein 1 (HMGB1). The temporal-spatial roles and potential therapeutics targeting this particular receptor-ligand interaction are also explored.
Division of Nephrology, Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390-8856, USA. Christopher.lu@utsouthwestern.edu
Christopher Y
CY
Lu
Pamela D
PD
Winterberg
Jianlin
J
Chen
John R
JR
Hartono
D058186:Acute Kidney Injury / Q000276:immunology* / Q000473:pathology; D000818:Animals; D042783:Endothelial Cells / Q000276:immunology* / Q000473:pathology; D024243:HMGB1 Protein / Q000378:metabolism; D006801:Humans; D007113:Immunity, Innate; D007249:Inflammation / Q000276:immunology; D007684:Kidney Tubules / Q000276:immunology* / Q000473:pathology; D007962:Leukocytes / Q000276:immunology* / Q000473:pathology; D008024:Ligands; D015398:Signal Transduction; D051197:Toll-Like Receptor 4 / Q000378:metabolism*
D024243:HMGB1 Protein; D008024:Ligands; D051197:Toll-Like Receptor 4