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...

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Published in:	Renal failure Vol. 44; no. 1; pp. 615 - 624
Main Authors:	Wang, Miao, Lin, Xin, Yang, Xiaoming, Yang, Yanlang
Format:	Journal Article
Language:	English
Published:	England Taylor & Francis 01.12.2022 Taylor & Francis Ltd Taylor & Francis Group
Subjects:	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
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Abstract	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.
AbstractList	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. 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.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.
Author	Lin, Xin Yang, Xiaoming Wang, Miao Yang, Yanlang
Author_xml	– sequence: 1 givenname: Miao surname: Wang fullname: Wang, Miao organization: Department of Nephrology, Yijishan Hospital of Wannan Medical College – sequence: 2 givenname: Xin surname: Lin fullname: Lin, Xin organization: Department of Nephrology, Yijishan Hospital of Wannan Medical College – sequence: 3 givenname: Xiaoming surname: Yang fullname: Yang, Xiaoming organization: Department of Nephrology, Yijishan Hospital of Wannan Medical College – sequence: 4 givenname: Yanlang surname: Yang fullname: Yang, Yanlang organization: Department of Nephrology, Yijishan Hospital of Wannan Medical College
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/35382689$$D View this record in MEDLINE/PubMed
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Snippet	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...
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SubjectTerms	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
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Title	Research progress on related mechanisms of uric acid activating NLRP3 inflammasome in chronic kidney disease
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