title: M1 macrophage triggered by Mincle leads to a deterioration of acute kidney injury.
abstract: In the early stage of acute kidney injury, M1 macrophages are proinflammatory and destructive. In this study, Lv et al. reveal that Mincle (macrophage-inducible C-type lectin, Clec4e) is expressed on M1 macrophages in acute kidney injury, and the kidney is protected in a murine model of cisplatin-induced renal injury by inhibiting Mincle expression on macrophages. Mincle expression is regulated by Toll-like receptor 4/nuclear factor κB signaling, and Mincle maintains the inflammatory phenotype through spleen tyrosine kinase signaling, leading to acute kidney injury.
authors.affiliation: Division of Nephrology and Center for Immunity, Inflammation, and Regenerative Medicine, University of Virginia, Charlottesville, Virginia, USA. Electronic address: Ti5s@virginia.edu.
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Inoue
mesh_terms: D058186:Acute Kidney Injury; D000818:Animals; D037181:Lectins, C-Type; D008264:Macrophages; D008565:Membrane Proteins; D051379:Mice; D051197:Toll-Like Receptor 4
chemical_list: D037181:Lectins, C-Type; D008565:Membrane Proteins; D051197:Toll-Like Receptor 4