Activation of hypoxia-inducible factor by cobalt is associated with the attenuation of tissue injury and apoptosis in cyclosporine-induced nephropathy

Keyphrases

• Attenuation 100%
• Apoptosis 100%
• Cobalt 100%
• Cyclosporine 100%
• Nephropathy 100%
• Hypoxia-inducible Factor 100%
• Tissue Injury 100%
• Kidney 27%
• Fibrosis 18%
• Hypoxia-inducible factor-1α (HIF-1α) 18%
• Apoptotic Cells 18%
• Transcription Factor 9%
• Infiltration 9%
• Therapeutic Benefits 9%
• Expression Level 9%
• NF-B 9%
• Phosphorylation 9%
• Inflammation 9%
• Macrophages 9%
• Induced Expression 9%
• Induced Apoptosis 9%
• Caspase-3 Activity 9%
• Animal Experiment 9%
• Monocytes 9%
• Pro-apoptotic 9%
• Clinical Application 9%
• α-smooth muscle Actin (α-SMA) 9%
• In Vitro Experiment 9%
• Vimentin 9%
• Cleaved caspase-3 9%
• Anti-apoptotic Bcl-2 9%
• Apoptosis Inflammation 9%
• Tubulointerstitium 9%
• Human Renal Tubular Epithelial Cells 9%
• HK-2 Cells 9%
• Organ Transplantation 9%
• Tubular Injury 9%
• Hypoxic Response 9%
• Low-salt Diet 9%
• Arteriolopathy 9%
• Apoptotic Caspases 9%
• Chronic Progressive Nephropathy 9%
• HK-2 9%

Pharmacology, Toxicology and Pharmaceutical Science

• Tissue Injury 100%
• Ciclosporin 100%
• Kidney Disease 100%
• Hypoxia Inducible Factor 100%
• Inflammation 18%
• Caspase 3 18%
• Fibrosis 18%
• Hypoxia Inducible Factor 1 18%
• Injury 9%
• Transcription Factors 9%
• Antiapoptotic 9%
• Smooth Muscle Actin 9%
• Vimentin 9%
• Chronic Kidney Failure 9%
• Table Salt 9%