Does inhibition of IκB Kinase β attenuate hypoxia-induced inflammatory mediators in rat renal tubular cells?
These data revealed that hypoxia-induced inflammatory responses were IKKβ/NF-κB-dependent. Knockdown of IKKβ by siRNA suppressed the transcription IKKβ/NF-κB-mediated inflammatory mediators in tumor necrosis factor-α or CoCl(2)-treated tubular epithelial cells, and decreased CoCl(2)-induced cell death, which may be a useful, preventive and therapeutic strategy for ischemic AKI.
Our findings clearly demonstrate elevations in cardiac fibrosis when type 1 diabetes is combined with hypertension. Our findings thus stress the importance of closely monitoring both blood pressure and glucose levels in type 1 diabetic patients in order to prevent myocardial collagen deposition.