TLR4 and HMGB1: Partners in crime

21Citations
Citations of this article
19Readers
Mendeley users who have this article in their library.

This article is free to access.

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. © 2011 International Society of Nephrology.

Cite

CITATION STYLE

APA

Goligorsky, M. S. (2011, September 1). TLR4 and HMGB1: Partners in crime. Kidney International. Nature Publishing Group. https://doi.org/10.1038/ki.2011.170

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free