TWEAK-Fn14 as a mediator of acute kidney injury.
Level V
Where this comes from
- Record sourced from PubMed, PMID 21191390.
- Also identified by DOI 10.1038/ki.2010.435 and PMC identifier 3125134.
- No licence information is recorded for this record.
- Because redistribution is not established, this page shows the abstract only. Follow the links below for the full text.
Abstract
Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor, fibroblast growth factor-inducible 14 (TWEAK-Fn14), are widely expressed and are involved in both injury and repair. Hotta et al. now demonstrate an important role for Fn14 in the common clamp ischemia model of acute kidney injury. Their data suggest paracrine and autocrine effects in which TWEAK produced by tubule cells feeds back on them via upregulated Fn-14 receptors expressed downstream in the proximal tubule.
Medical subject headings
- Acute Kidney Injury
- Receptors, Tumor Necrosis Factor
- Tumor Necrosis Factors