Research progress on related mechanisms of uric acid activating NLRP3 inflammasome in chronic kidney disease

Hyperuricemia is an independent risk factor for the progression of chronic kidney disease. High levels of uric acid can lead to a series of pathological conditions, such as gout, urinary stones, inflammation, and uric acid nephropathy. There is a close relationship between uric acid and the NLRP3 in...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Renal failure Jg. 44; H. 1; S. 615 - 624
Hauptverfasser: Wang, Miao, Lin, Xin, Yang, Xiaoming, Yang, Yanlang
Format: Journal Article
Sprache:Englisch
Veröffentlicht: England Taylor & Francis 01.12.2022
Taylor & Francis Ltd
Taylor & Francis Group
Schlagworte:
Caspase-1
Cell activation
Cell death
Cell membranes
Crystals
Endoplasmic reticulum
Golgi apparatus
Gout
Humans
Hyperuricemia
Hyperuricemia - complications
Inflammasomes
Inflammasomes - metabolism
Inflammation
Interleukin 18
Interleukin-1beta - metabolism
Kidney diseases
Lysis
Mitochondria
Molecular modelling
Nephropathy
NLR Family, Pyrin Domain-Containing 3 Protein - metabolism
NLRP3 inflammasomes
organelle
oxidative stress
Renal Insufficiency, Chronic - etiology
Review
Risk factors
State-of-the-Art Review
Uric acid
Uric Acid - metabolism
NLRP3 inflammasomes
Uric acid
organelle
oxidative stress
ISSN:0886-022X, 1525-6049, 1525-6049
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:Hyperuricemia is an independent risk factor for the progression of chronic kidney disease. High levels of uric acid can lead to a series of pathological conditions, such as gout, urinary stones, inflammation, and uric acid nephropathy. There is a close relationship between uric acid and the NLRP3 inflammasome. NLRP3 inflammasome activation can cause cell damage and even death through endoplasmic reticulum stress, lysosome destruction, mitochondrial dysfunction, and the interaction between the Golgi apparatus and extracellular vesicles. In addition, the NLRP3 inflammasome acts as a molecular platform, triggering the activation of caspase-1 and the lysis of IL-1β, IL-18 and Gasdermin D (GSDMD) through different molecular mechanisms. Cleaved NT-GSDMD forms pores in the cell membrane and triggers pyrophosphorylation, thereby inducing cell death and releasing many intracellular proinflammatory molecules. In recent years, studies have found that hyperuricemia or uric acid crystals can activate NLRP3 inflammasomes, and the activation of NLRP3 inflammasomes plays an important role in kidney disease. This article reviews the possible pathophysiological mechanisms by which uric acid activates inflammasomes and induces kidney damage at the cellular and molecular levels.
Bibliographie:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
ObjectType-Review-3
content type line 23
ISSN:0886-022X
1525-6049
1525-6049
DOI:10.1080/0886022X.2022.2036620