title: A remedy for kidney disease successfully alters the cold shock protein response during inflammation.
abstract: Kidneys undergoing acute inflammatory responses are characterized by cell infiltration and a cytokinergic milieu. The hazard resides in the perpetuation of inflammation and ensuing fibrosis. In this issue of Kidney International, Wang et al.4identify the cold shock Y-box binding protein-1 as the key orchestrator of cell infiltration in experimental tubulointerstitial nephritis following ureteral obstruction. Intriguingly, a small molecule previously designed to interfere with Y-box binding protein-1 interactions mediates an anti-inflammatory response and halts fibrogenesis.
authors.affiliation: Clinic of Nephrology and Hypertension, Diabetes and Endocrinology, Otto-von-Guericke University Magdeburg, Germany.
authors.forename: Sabine
authors.initials: S
authors.lastname: Brandt
authors.affiliation: Clinic of Nephrology and Hypertension, Diabetes and Endocrinology, Otto-von-Guericke University Magdeburg, Germany. Electronic address: peter.mertens@med.ovgu.de.
authors.forename: Peter R
authors.initials: PR
authors.lastname: Mertens
mesh_terms: D057773:Cold Shock Proteins and Peptides; D058639:Cold-Shock Response; D005355:Fibrosis; D006801:Humans; D007249:Inflammation; D007668:Kidney; D014517:Ureteral Obstruction
chemical_list: D057773:Cold Shock Proteins and Peptides