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.