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M1 macrophage triggered by Mincle leads to a deterioration of acute kidney injury
Author(s) -
Tsuyoshi Inoue
Publication year - 2017
Publication title -
kidney international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.499
H-Index - 276
eISSN - 1523-1755
pISSN - 0085-2538
DOI - 10.1016/j.kint.2016.11.026
Subject(s) - acute kidney injury , proinflammatory cytokine , medicine , kidney disease , kidney , immunology , cancer research , pathology , inflammation
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.

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