title: TWEAK-Fn14 as a mediator of acute kidney injury.
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.
authors.affiliation: Division of Nephrology, Department of Internal Medicine, Veterans Affairs Ann Arbor Healthcare System and University of Michigan, Ann Arbor, Michigan, USA. wnberg@umich.edu
authors.forename: Joel M
authors.initials: JM
authors.lastname: Weinberg
mesh_terms: D058186:Acute Kidney Injury / Q000209:etiology* / Q000503:physiopathology; D000818:Animals; D019898:Autocrine Communication; D000074049:Cytokine TWEAK; D025461:Feedback, Physiological; D051379:Mice; D019899:Paracrine Communication; D018124:Receptors, Tumor Necrosis Factor / Q000502:physiology*; D000074050:TWEAK Receptor; D048069:Tumor Necrosis Factors / Q000502:physiology*
chemical_list: D000074049:Cytokine TWEAK; D018124:Receptors, Tumor Necrosis Factor; D000074050:TWEAK Receptor; C000613299:Tnfrsf12a protein, mouse; C491645:Tnfsf12 protein, mouse; D048069:Tumor Necrosis Factors