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Título: | NF-κB in renal inflammation |
Autor: | Santamaria, Beatriz CSIC ORCID; Ortiz, Alberto | Fecha de publicación: | 2010 | Editor: | American Society of Nephrology | Citación: | Journal of the American Society of Nephrology 21(8): 1254-1262 (2010) | Resumen: | The NF-κB family of transcription factors regulates the induction and resolution of inflammation. Two main pathways, classical and alternative, control the nuclear translocation of NF-κB. Classical NF-κB activation is usually a rapid and transient response to a wide range of stimuli whose main effector is RelA/p50. The alternative NF-κB 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-κB proteins and an ever-increasing range of co-activators, co-repressors, and NF-κB complex proteins. Collectively, NF-κB regulates the expression of numerous genes that play a key role in the inflammatory response during human and experimental kidney injury. Multiple stimuli activate NF-κB 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-κB inhibitors tend to reduce inflammation in experimental kidney injury but not always. Although many drugs in current use clinically influence NF-κB activation, there are no data regarding specific NF-κB inhibition in human kidney disease. Copyright © 2010 by the American Society of Nephrology. | URI: | http://hdl.handle.net/10261/77463 | DOI: | 10.1681/ASN.2010020218 | Identificadores: | doi: 10.1681/ASN.2010020218 issn: 1046-6673 e-issn: 1533-3450 |
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