期刊
KIDNEY INTERNATIONAL
卷 80, 期 5, 页码 450-452出版社
ELSEVIER SCIENCE INC
DOI: 10.1038/ki.2011.170
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资金
- NIDDK NIH HHS [DK45462, DK052783, R01 DK084394, DK54602] Funding Source: Medline
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. Kidney International (2011) 80, 450-452. doi:10.1038/ki.2011.170
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