Kathryn M. Oliver

TL;DR: It is hypothesized that hypoxia enhances NF-kappaB activity primarily through affecting the canonical pathway, and in synovial biopsies obtained at arthroscopy from patients with active inflammatory arthritis, the canonical pathways was preferentially activated in those patents with lower joint pO2 values.

TL;DR: It is demonstrated that mammalian cells also sense changes in local CO2 levels, leading to altered gene expression via the NF-κB pathway, suggesting the existence of a molecular CO2 sensor in mammalian cells that is linked to the regulation of genes involved in innate immunity and inflammation.

TL;DR: The present review will discuss recent literature pertaining to the regulation of NFκB inflammatory signalling by hypoxia and some of the inflammatory diseases where this may play an important role and the potential for prolylhydroxylase inhibitors in inflammatory disease.

TL;DR: It is demonstrated that in cells exposed to elevated CO2, the NF-κB family member RelB was cleaved to a lower molecular weight form and translocated to the nucleus in both mouse embryonic fibroblasts and human pulmonary epithelial cells.

TL;DR: In this paper, a review of the literature pertaining to the regulation of NFκB inflammatory signalling by hypoxia and some of the inflammatory diseases where this may play an important role is presented.