TWEAK/Fn14 and non-canonical NF-kappaB signaling in kidney disease
Entity
UAM. Departamento de Medicina; Instituto de Investigación Sanitaria Fundación Jiménez Díaz (IIS-FJD)Publisher
FrontiersDate
2013-12-10Citation
10.3389/fimmu.2013.00447
Frontiers in Immunology 4.447 (2013)
ISSN
1664-3224DOI
10.3389/fimmu.2013.00447Funded by
Grant support: ISCII and FEDER funds FIS PS09/00447, ISCIII-RETIC REDinREN/RD06/0016, RD12/0021, Comunidad de Madrid/CIFRA/S2010/BMD-2378. Salary support: FIS to MDSN, Programa Intensificación Actividad Investigadora (ISCIII/Agencia Laín-Entralgo/CM) to AO, FPU (Ministerio de Educación, Cultura y Deporte) to JP, Fundacion Conchita Rabago to LCT.Project
Comunidad de Madrid. S2010/BMD-2378/CIFRAEditor's Version
http://dx.doi.org/10.3389/fimmu.2013.00447Subjects
Kidneys; TWEAK/Fn14; Inflammation; MedicinaRights
© 2013 Poveda, Tabara, Fernandez-Fernandez, Martin-Cleary, Sanz, Selgas, Ortiz and Sanchez-Niño.Abstract
The incidence of acute kidney injury (AKI) and chronic kidney disease (CKD) is increasing. However, there is no effective therapy for AKI and current approaches only slow down, but do not prevent progression of CKD. TWEAK is a TNF superfamily cytokine. A solid base of preclinical data suggests a role of therapies targeting the TWEAK or its receptor Fn14 in AKI and CKD. In particular TWEAK/Fn14 targeting may preserve renal function and decrease cell death, inflammation, proteinuria, and fibrosis in mouse animal models. Furthermore there is clinical evidence for a role of TWEAK in human kidney injury including increased tissue and/or urinary levels of TWEAK and parenchymal renal cell expression of the receptor Fn14. In this regard, clinical trials of TWEAK targeting are ongoing in lupus nephritis. Nuclear factor-kappa B (NF-κB) activation plays a key role in TWEAK-elicited inflammatory responses. Activation of the non-canonical NF-κB pathway is a critical difference between TWEAK and TNF. TWEAK activation of the non-canonical NF-κB pathways promotes inflammatory responses in tubular cells. However, there is an incomplete understanding of the role of non-canonical NF-κB activation in kidney disease and on its contribution to TWEAK actions in vivo.
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Google Scholar:Poveda, Jonay
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Tabara, Luis C.
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Fernández-Fernández, Beatriz
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Mart, Catalina
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Sanz, Ana Belén
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Selgas, Rafael
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Ortiz Arduán, Alberto
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Sánchez Niño, María Dolores
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