ReferenceID 174

The inflammatory cytokines TWEAK and TNFα reduce renal klotho expression through NFκB

J Am Soc Nephrol

Proinflammatory cytokines contribute to renal injury, but the downstream effectors within kidney cells are not well understood. One candidate effector is Klotho, a protein expressed by renal cells that has antiaging pro

Back to Browse

Relationship Network

Interactive first-hop connections across herbs, ingredients, formulas, targets, diseases, symptoms, syndromes, evidence, and monographs.

Click a node to open it in a new tab
Ingredient: 1Reference: 1Links: 1
Arranging relationship network...

Record Fields

Scalar fields from the final reference record.

Reference Id
174
Evidence Id
16764
Core Evidence Id
16764
Source Reference Id
310
Herb2 Reference Id
HBREF000571
Subject Paper Key
HBIN038876_21719790
Pubmed Id
21719790
Doi
10.1681/ASN.2010101073
Paper Title
The inflammatory cytokines TWEAK and TNFα reduce renal klotho expression through NFκB
Paper Abstract
Proinflammatory cytokines contribute to renal injury, but the downstream effectors within kidney cells are not well understood. One candidate effector is Klotho, a protein expressed by renal cells that has antiaging properties; Klotho-deficient mice have an accelerated aging-like phenotype, including vascular injury and renal injury. Whether proinflammatory cytokines, such as TNF and TNF-like weak inducer of apoptosis (TWEAK), modulate Klotho is unknown. In mice, exogenous administration of TWEAK decreased expression of Klotho in the kidney. In the setting of acute kidney injury induced by folic acid, the blockade or absence of TWEAK abrogated the injury-related decrease in renal and plasma Klotho levels. TWEAK, TNFα, and siRNA-mediated knockdown of IκBα all activated NFκB and reduced Klotho expression in the MCT tubular cell line. Furthermore, inhibition of NFκB with parthenolide prevented TWEAK- or TNFα-induced downregulation of Klotho. Inhibition of histone deacetylase reversed TWEAK-induced downregulation of Klotho, and chromatin immunoprecipitation showed that TWEAK promotes RelA binding to the Klotho promoter, inducing its deacetylation. In conclusion, inflammatory cytokines, such as TWEAK and TNFα, downregulate Klotho expression through an NFκB-dependent mechanism. These results may partially explain the relationship between inflammation and diseases characterized by accelerated aging of organs, including CKD.
Journal
J Am Soc Nephrol
Publish Year
2011
Experiment Subject
klotho-deficient mice
Experiment Type
Animal Experiment
Phenotype Related
Paper Title Cn
Paper Title En
The inflammatory cytokines TWEAK and TNFα reduce renal klotho expression through NFκB
Bilingual Status
semi_complete