title: Hyperuricemia-induced inflammasome and kidney diseases.
abstract: Classically, urate nephropathy has been postulated to cause kidney disease by depositing intraluminal crystal in the collecting duct. Recently, molecular mechanisms of inflammasome have been investigated. Urate-induced inflammasome pathway is comprised of urate crystal uptake into intracellular lysosomes and subsequent lysosomal rupture with mitochondrial reactive oxygen species (ROS) production, which activates the NLRP3 inflammasome. Against the lysosomal rupture and mitochondrial ROS production, autophagy acts to protect proximal tubular cells by isolating them from expanding the inflammation. In addition, increased cellular urate, directly or indirectly via xanthine oxidase-induced oxidative stress, may be associated with inflammasome. In addition to the traditional therapy against hyperuricemia, management of urate-induced inflammasome or augmentation of autophagy may offer the new effective therapies.
authors.affiliation: Department of Geriatric Medicine and Nephrology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
authors.forename: Yoshitaka
authors.initials: Y
authors.lastname: Isaka
authors.affiliation: Department of Geriatric Medicine and Nephrology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
authors.forename: Yoshitsugu
authors.initials: Y
authors.lastname: Takabatake
authors.affiliation: Department of Geriatric Medicine and Nephrology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
authors.forename: Atsushi
authors.initials: A
authors.lastname: Takahashi
authors.affiliation: Laboratory of Host Defense, World Premier International Research Center Immunology Frontier Research Center, Osaka University, Osaka, Japan Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Saitoh
authors.affiliation: Department of Genetics, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
authors.forename: Tamotsu
authors.initials: T
authors.lastname: Yoshimori
mesh_terms: D000818:Animals; D006801:Humans; D033461:Hyperuricemia / Q000150:complications* / Q000503:physiopathology; D058847:Inflammasomes / Q000378:metabolism*; D007249:Inflammation / Q000209:etiology* / Q000503:physiopathology; D007674:Kidney Diseases / Q000209:etiology* / Q000503:physiopathology
chemical_list: D058847:Inflammasomes
keywords: autophagy; lysosome; mitochondria