期刊
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
卷 21, 期 8, 页码 1254-1262出版社
AMER SOC NEPHROLOGY
DOI: 10.1681/ASN.2010020218
关键词
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资金
- EU [LSHB-CT-2007-036644, ISCIII-RETIC REDinREN/RD06/0016]
- [FIS 06/0046]
- [PS09/00447]
- [CP07/0020]
- [PI08/1083]
- [PI081564]
The NF-kappa B family of transcription factors regulates the induction and resolution of inflammation. Two main pathways, classical and alternative, control the nuclear translocation of NF-kappa B. Classical NF-kappa B activation is usually a rapid and transient response to a wide range of stimuli whose main effector is RelA/p50. The alternative NF-kappa B pathway is a more delayed response to a smaller range of stimuli resulting in DNA binding of RelB/p52 complexes. Additional complexity in this system involves the posttranslational modification of NF-kappa B proteins and an ever-increasing range of co-activators, co-repressors, and NF-kappa B complex proteins. Collectively, NF-kappa B regulates the expression of numerous genes that play a key role in the inflammatory response during human and experimental kidney injury. Multiple stimuli activate NE-kappa B through the classical pathway in somatic renal cells, and noncanonical pathway activation by TWEAK occurs in acute kidney injury. Under most test conditions, specific NF-kappa B inhibitors tend to reduce inflammation in experimental kidney injury but not always. Although many drugs in current use clinically influence NF-kappa B activation, there are no data regarding specific NF-kappa B inhibition in human kidney disease.
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