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TRAIL, OPG, and TWEAK in kidney disease: biomarkers or therapeutic targets?

Authors :
Bernardi, Stella
Voltan, Rebecca
Rimondi, Erika
Melloni, Elisabetta
Milani, Daniela
Cervellati, Carlo
Gemmati, Donato
Celeghini, Claudio
Secchiero, Paola
Zaul, Giorgio
Tisato, Veronica
Source :
Clinical Science. 5/31/2019, Vol. 133 Issue 10, p1145-1166. 22p.
Publication Year :
2019

Abstract

Ligands and receptors of the tumor necrosis factor (TNF) superfamily regulate immune responses and homeostatic functions with potential diagnostic and therapeutic implications. Kidney disease represents a global public health problem, whose prevalence is rising worldwide, due to the aging of the population and the increasing prevalence of diabetes, hypertension, obesity, and immune disorders. In addition, chronic kidney disease is an independent risk factor for the development of cardiovascular disease, which further increases kidney-related morbidity and mortality. Recently, it has been shown that some TNF superfamily members are actively implicated in renal pathophysiology. These members include TNF-related apoptosis-inducing ligand (TRAIL), its decoy receptor osteoprotegerin (OPG), and TNF-like weaker inducer of apoptosis (TWEAK). All of them have shown the ability to activate crucial pathways involved in kidney disease development and progression (e.g. canonical and non-canonical pathways of the transcription factor nuclear factor-kappa B), as well as the ability to regulate cell proliferation, differentiation, apoptosis, necrosis, inflammation, angiogenesis, and fibrosis with double-edged effects depending on the type and stage of kidney injury. Here we will review the actions of TRAIL, OPG, and TWEAK on diabetic and non-diabetic kidney disease, in order to provide insights into their full clinical potential as biomarkers and/or therapeutic options against kidney disease. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
01435221
Volume :
133
Issue :
10
Database :
Academic Search Index
Journal :
Clinical Science
Publication Type :
Academic Journal
Accession number :
136779053
Full Text :
https://doi.org/10.1042/CS20181116