A remedy for kidney disease successfully alters the cold shock protein response during inflammation.
Level V
Where this comes from
- Record sourced from PubMed, PMID 27884304.
- Also identified by DOI 10.1016/j.kint.2016.07.041.
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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.<sup>4</sup> identify 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.
Medical subject headings
- Cold Shock Proteins and Peptides
- Ureteral Obstruction