title: TLR4 and HMGB1: partners in crime?
abstract: Chen et al. confirmed the role of Toll-like receptor 4 (TLR4) in ischemic kidney injury using mice harboring spontaneous disabling mutations of the receptor and generated chimeras between TLR4-/- and TLR4+/+ mice. The major findings demonstrate the necessity of TLR4 in leukocytes, as well as in epithelial and endothelial cells, for the full-blown ischemic response and strongly suggest that the release of high-mobility group box 1 protein (HMGB1) from injured epithelia and/or endothelia activates leukocytes to generate proinflammatory cytokines, further exacerbating the injury to ischemic kidneys. These important findings provide an excellent platform for discussing the complexity of danger/alarm signaling in the kidney.
authors.affiliation: Department of Medicine, Renal Research Institute, New York Medical College, Valhalla, New York 10595, USA. michael_goligorsky@nymc.edu
authors.forename: Michael S
authors.initials: MS
authors.lastname: Goligorsky
mesh_terms: D058186:Acute Kidney Injury / Q000276:immunology*; D000818:Animals; D015850:Interleukin-6 / Q000096:biosynthesis*; D007962:Leukocytes / Q000378:metabolism*; D008297:Male; D051197:Toll-Like Receptor 4 / Q000502:physiology*
chemical_list: D015850:Interleukin-6; C493487:Tlr4 protein, mouse; D051197:Toll-Like Receptor 4