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...

Full description

Saved in:

Bibliographic Details
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
Online Access:	Get full text
Tags:	Add Tag No Tags, Be the first to tag this record!

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
BookMark	eNqFktuKFDEQhhtZcQ_6CEqDN97MmnN3I4iyeFgYVBYF70J1UpnJ2J2MSc_KvL0ZZ3Zx90JvKiT56k-q6j-tjkIMWFVPKTmnpCUvSdsqwtj3c1ZiCVwpRh5UJ1QyOVNEdEfVyY6Z7aDj6jTnFSFUtg17VB1zyVum2u6kGq4wIySzrNcpLhLmXMdQJxxgQluPaJYQfB7Lqas3yZsajLclTP4aJh8W9af51Rde--AGGEfIccSyqc0yxVDoH94G3NbWl0cyPq4eOhgyPjmsZ9W39---XnyczT9_uLx4O58Zqdg0s86ynotGobS0ZWhJwwCE6biSjjfOGdqgEQysEyBbwUUPHVBFlUTbcORn1eVe10ZY6XXyI6StjuD1n4OYFhrS5M2Auu-VbSiBznAirOt65QwRHAVFgaqlRev1Xmu96Ue0BsOUYLgjevcm-KVexGvdESIka4rAi4NAij83mCc9-mxwGCBg3GTNVKm01N2Jgj6_h67iJoXSKs2alqjSByUL9ezvH91-5WaoBZB7wKSYc0J3i1Cid-bRN-bRO_Pog3lK3qt7ecZPZcpxV5gf_pv9Zp9dvBDTCL9iGqyeYDvE5BIE47Pm_5b4DexB3oI
CitedBy_id	crossref_primary_10_3390_ph18050762 crossref_primary_10_1093_ckj_sfae235 crossref_primary_10_1111_aos_16646 crossref_primary_10_3390_nu17101679 crossref_primary_10_3390_microorganisms13061367 crossref_primary_10_1097_MD_0000000000036732 crossref_primary_10_1089_jmf_2023_K_0268 crossref_primary_10_1038_s41392_024_01916_y crossref_primary_10_1111_cbdd_14367 crossref_primary_10_1016_j_imlet_2023_11_003 crossref_primary_10_1016_j_ejphar_2023_175931 crossref_primary_10_1016_j_jare_2025_08_031 crossref_primary_10_1016_j_biopha_2022_113746 crossref_primary_10_1016_j_jff_2023_105903 crossref_primary_10_3389_fnut_2024_1335074 crossref_primary_10_1080_0886022X_2025_2504634 crossref_primary_10_2147_JIR_S525351 crossref_primary_10_3389_fsurg_2022_956213 crossref_primary_10_3892_ijmm_2024_5376 crossref_primary_10_3389_fmed_2025_1623557 crossref_primary_10_3390_biomedicines11092353 crossref_primary_10_1111_1756_185X_70096 crossref_primary_10_3390_jcm14134606 crossref_primary_10_1016_j_isci_2023_108463 crossref_primary_10_1016_j_jep_2023_116530 crossref_primary_10_1016_j_jdiacomp_2024_108929 crossref_primary_10_1016_j_jrras_2023_100626 crossref_primary_10_3389_fncel_2022_1013450 crossref_primary_10_1292_jvms_23_0085 crossref_primary_10_1016_j_fbio_2024_104136 crossref_primary_10_3390_fermentation9040352 crossref_primary_10_1016_j_biopha_2022_114199 crossref_primary_10_1016_j_phymed_2025_156974 crossref_primary_10_3390_ijms26189000 crossref_primary_10_1016_j_jep_2023_117262 crossref_primary_10_1186_s12872_023_03333_5 crossref_primary_10_1097_MD_0000000000038210 crossref_primary_10_1002_iid3_1062 crossref_primary_10_1002_bmc_70035 crossref_primary_10_1016_j_microc_2025_113762 crossref_primary_10_1021_acs_jafc_4c08428 crossref_primary_10_1016_j_bmc_2024_117874 crossref_primary_10_2147_DDDT_S516001 crossref_primary_10_1016_j_jep_2024_118606 crossref_primary_10_1007_s00240_024_01606_y crossref_primary_10_1016_j_cellsig_2024_111256 crossref_primary_10_1016_j_gene_2025_149256
Cites_doi	10.3892/ijmm.2016.2491 10.1016/j.mito.2017.10.009 10.1038/s41586-018-0761-3 10.1038/s41419-018-1157-x 10.1096/fj.15-271734 10.1038/s41586-018-0372-z 10.1096/fj.201801585R 10.4049/jimmunol.1201959 10.1161/ATVBAHA.119.313224 10.1016/j.redox.2015.01.008 10.4049/jimmunol.1900228 10.3899/jrheum.180855 10.1038/nature11588 10.1186/ar3898 10.1074/jbc.M112.407130 10.1016/j.mrfmmm.2018.09.001 10.1007/s10571-020-00855-w 10.1016/j.biopha.2018.10.129 10.4049/jimmunol.1201946 10.1080/14397595.2020.1740410 10.1038/srep39884 10.1038/s41577-019-0165-0 10.1136/annrheumdis-2014-206564 10.1159/000345509 10.1038/ni.2550 10.1016/j.ijbiomac.2020.07.060 10.1155/2015/535686 10.1038/s12276-019-0254-y 10.1084/jem.20162040 10.12659/MSM.916667 10.1016/j.bbamcr.2019.02.007 10.1016/j.bcp.2020.113998 10.1038/ni.1831 10.1016/j.immuni.2015.08.008 10.3390/cells9020279 10.1159/000488048 10.3390/antiox9050387 10.4049/jimmunol.1701723 10.3892/ijmm.2015.2148 10.1002/jcb.26806 10.1155/2017/8316560 10.1155/2018/7635274 10.1016/j.freeradbiomed.2018.08.011 10.1074/jbc.M113.470971 10.3389/fcell.2020.00167 10.1080/0886022X.2019.1633350 10.1016/j.bbrc.2019.02.141 10.1038/s41598-019-42130-z 10.1002/bab.1700 10.1186/s12882-019-1506-8 10.1016/j.bbrc.2017.02.019 10.1074/mcp.M112.024661 10.1007/s12020-014-0239-5 10.3389/fimmu.2018.00316 10.1007/s10157-019-01705-w 10.1016/j.phymed.2019.153111 10.1159/000484274 10.1016/j.cell.2015.12.057 10.1083/jcb.201709057
ContentType	Journal Article
Copyright	2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. 2022 2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. This work is licensed under the Creative Commons Attribution License http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. 2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. 2022 The Author(s)
Copyright_xml	– notice: 2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. 2022 – notice: 2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. This work is licensed under the Creative Commons Attribution License http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. – notice: 2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. 2022 The Author(s)
DBID	0YH AAYXX CITATION CGR CUY CVF ECM EIF NPM 3V. 7T5 7X7 7XB 88E 8FI 8FJ 8FK 8G5 ABUWG AFKRA AZQEC BENPR CCPQU DWQXO FYUFA GHDGH GNUQQ GUQSH H94 K9. M0S M1P M2O MBDVC PHGZM PHGZT PIMPY PJZUB PKEHL PPXIY PQEST PQQKQ PQUKI PRINS Q9U 7X8 5PM DOA
DOI	10.1080/0886022X.2022.2036620
DatabaseName	Taylor & Francis Open Access CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed ProQuest Central (Corporate) Immunology Abstracts ProQuest Health & Medical Collection ProQuest Central (purchase pre-March 2016) Medical Database (Alumni Edition) Hospital Premium Collection Hospital Premium Collection (Alumni Edition) ProQuest Central (Alumni) (purchase pre-March 2016) Research Library (Alumni Edition) ProQuest Central (Alumni) ProQuest Central UK/Ireland ProQuest Central Essentials ProQuest Central ProQuest One Community College ProQuest Central Health Research Premium Collection Health Research Premium Collection (Alumni) ProQuest Central Student Research Library Prep AIDS and Cancer Research Abstracts ProQuest Health & Medical Complete (Alumni) Health & Medical Collection (Alumni Edition) PML(ProQuest Medical Library) Research Library Research Library (Corporate) ProQuest Central Premium ProQuest One Academic (New) Publicly Available Content Database ProQuest Health & Medical Research Collection ProQuest One Academic Middle East (New) ProQuest One Health & Nursing ProQuest One Academic Eastern Edition (DO NOT USE) ProQuest One Academic (retired) ProQuest One Academic UKI Edition ProQuest Central China ProQuest Central Basic MEDLINE - Academic PubMed Central (Full Participant titles) DOAJ Directory of Open Access Journals
DatabaseTitle	CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) Publicly Available Content Database Research Library Prep ProQuest Central Student ProQuest One Academic Middle East (New) ProQuest Central Essentials ProQuest Health & Medical Complete (Alumni) ProQuest Central (Alumni Edition) ProQuest One Community College ProQuest One Health & Nursing Research Library (Alumni Edition) ProQuest Central China ProQuest Central ProQuest Health & Medical Research Collection Health Research Premium Collection Health and Medicine Complete (Alumni Edition) ProQuest Central Korea Health & Medical Research Collection AIDS and Cancer Research Abstracts ProQuest Research Library ProQuest Central (New) ProQuest Medical Library (Alumni) ProQuest Central Basic ProQuest One Academic Eastern Edition ProQuest Hospital Collection Health Research Premium Collection (Alumni) ProQuest Hospital Collection (Alumni) ProQuest Health & Medical Complete ProQuest Medical Library ProQuest One Academic UKI Edition Immunology Abstracts ProQuest One Academic ProQuest One Academic (New) ProQuest Central (Alumni) MEDLINE - Academic
DatabaseTitleList	MEDLINE Publicly Available Content Database MEDLINE - Academic
Database_xml	– sequence: 1 dbid: DOA name: DOAJ Directory of Open Access Journals url: https://www.doaj.org/ sourceTypes: Open Website – sequence: 2 dbid: NPM name: PubMed url: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 3 dbid: 0YH name: Taylor & Francis Open Access url: https://www.tandfonline.com sourceTypes: Publisher – sequence: 4 dbid: PIMPY name: Publicly Available Content Database url: http://search.proquest.com/publiccontent sourceTypes: Aggregation Database
DeliveryMethod	fulltext_linktorsrc
Discipline	Medicine
DocumentTitleAlternate	M. Wang et al
EISSN	1525-6049
EndPage	624
ExternalDocumentID	oai_doaj_org_article_bb6d710a9c304df9b6fc043e41e4e681 PMC9004527 35382689 10_1080_0886022X_2022_2036620 2036620
Genre	Review Journal Article
GroupedDBID	--- 00X 0YH 123 29P 36B 4.4 53G 5RE 7X7 88E 8FI 8FJ 8G5 ABDBF ABUWG ACGEJ ACGFS ACUHS ADBBV ADCVX ADRBQ ADXPE AENEX AFKRA AFKVX AJWEG ALMA_UNASSIGNED_HOLDINGS AOIJS AQTUD ARJSQ AZQEC BABNJ BCNDV BENPR BLEHA CCPQU CS3 DWQXO EAP EBC EBD EBS EMB EMK EMOBN EPL ESX F5P FYUFA GNUQQ GROUPED_DOAJ GUQSH H13 HMCUK HZ~ M1P M2O M4Z O9- P2P PHGZM PHGZT PIMPY PJZUB PPXIY PROAC PSQYO RPM SV3 TDBHL TFDNU TFL TFW TUS UKHRP V1S ~1N AAYXX AFFHD CITATION .GJ 5VS AALIY AAORF AAPXX ABWCV AFLEI AJVHN AWYRJ BPHCQ BRMBE CAG CGR COF CUY CVF CYYVM CZDIS DRXRE DWTOO ECM EIF EJD HYE JENTW M44 NPM NUSFT OK1 PQQKQ QQXMO ZGI ZXP 3V. 7T5 7XB 8FK H94 K9. MBDVC PKEHL PQEST PQUKI PRINS Q9U 7X8 PUEGO 5PM
ID	FETCH-LOGICAL-c562t-dfd2b3476e5d182ed072aa4c9365f37ffc17ec42adf4a58434ba9a16165ed73e3
IEDL.DBID	DOA
ISICitedReferencesCount	59
ISICitedReferencesURI	http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=000779448300001&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
ISSN	0886-022X 1525-6049
IngestDate	Mon Nov 10 04:27:51 EST 2025 Tue Nov 04 01:57:03 EST 2025 Wed Oct 01 13:59:12 EDT 2025 Tue Oct 07 06:59:48 EDT 2025 Thu Jan 02 22:54:54 EST 2025 Tue Nov 18 20:41:40 EST 2025 Sat Nov 29 02:26:01 EST 2025 Mon Oct 20 23:46:15 EDT 2025
IsDoiOpenAccess	true
IsOpenAccess	true
IsPeerReviewed	true
IsScholarly	true
Issue	1
Keywords	NLRP3 inflammasomes Uric acid organelle oxidative stress
Language	English
License	open-access: http://creativecommons.org/licenses/by/4.0/: This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
LinkModel	DirectLink
MergedId	FETCHMERGED-LOGICAL-c562t-dfd2b3476e5d182ed072aa4c9365f37ffc17ec42adf4a58434ba9a16165ed73e3
Notes	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 ObjectType-Review-3 content type line 23
OpenAccessLink	https://doaj.org/article/bb6d710a9c304df9b6fc043e41e4e681
PMID	35382689
PQID	2780607265
PQPubID	3933335
PageCount	10
ParticipantIDs	pubmedcentral_primary_oai_pubmedcentral_nih_gov_9004527 crossref_primary_10_1080_0886022X_2022_2036620 proquest_miscellaneous_2647656294 pubmed_primary_35382689 crossref_citationtrail_10_1080_0886022X_2022_2036620 informaworld_taylorfrancis_310_1080_0886022X_2022_2036620 doaj_primary_oai_doaj_org_article_bb6d710a9c304df9b6fc043e41e4e681 proquest_journals_2780607265
PublicationCentury	2000
PublicationDate	2022-Dec
PublicationDateYYYYMMDD	2022-12-01
PublicationDate_xml	– month: 12 year: 2022 text: 2022-Dec
PublicationDecade	2020
PublicationPlace	England
PublicationPlace_xml	– name: England – name: New York
PublicationTitle	Renal failure
PublicationTitleAlternate	Ren Fail
PublicationYear	2022
Publisher	Taylor & Francis Taylor & Francis Ltd Taylor & Francis Group
Publisher_xml	– name: Taylor & Francis – name: Taylor & Francis Ltd – name: Taylor & Francis Group
References	e_1_3_2_28_1 e_1_3_2_49_1 e_1_3_2_20_1 e_1_3_2_41_1 e_1_3_2_22_1 e_1_3_2_43_1 e_1_3_2_24_1 e_1_3_2_45_1 e_1_3_2_26_1 e_1_3_2_47_1 e_1_3_2_62_1 e_1_3_2_60_1 e_1_3_2_16_1 e_1_3_2_39_1 e_1_3_2_9_1 e_1_3_2_18_1 e_1_3_2_7_1 Wang GL (e_1_3_2_51_1) 2018; 49 e_1_3_2_31_1 e_1_3_2_54_1 e_1_3_2_10_1 e_1_3_2_33_1 e_1_3_2_52_1 e_1_3_2_12_1 e_1_3_2_35_1 e_1_3_2_58_1 e_1_3_2_5_1 e_1_3_2_14_1 e_1_3_2_37_1 e_1_3_2_56_1 e_1_3_2_3_1 Haryono A (e_1_3_2_2_1) 2018; 64 e_1_3_2_50_1 Bhatia D (e_1_3_2_21_1) 2019; 1 e_1_3_2_27_1 e_1_3_2_29_1 e_1_3_2_42_1 e_1_3_2_44_1 e_1_3_2_63_1 e_1_3_2_23_1 e_1_3_2_46_1 e_1_3_2_25_1 e_1_3_2_48_1 e_1_3_2_61_1 e_1_3_2_40_1 e_1_3_2_17_1 e_1_3_2_38_1 e_1_3_2_8_1 e_1_3_2_19_1 e_1_3_2_30_1 e_1_3_2_55_1 e_1_3_2_11_1 e_1_3_2_32_1 e_1_3_2_53_1 e_1_3_2_6_1 e_1_3_2_13_1 e_1_3_2_34_1 e_1_3_2_59_1 e_1_3_2_4_1 e_1_3_2_15_1 e_1_3_2_36_1 e_1_3_2_57_1
References_xml	– ident: e_1_3_2_29_1 doi: 10.3892/ijmm.2016.2491 – ident: e_1_3_2_19_1 doi: 10.1016/j.mito.2017.10.009 – ident: e_1_3_2_33_1 doi: 10.1038/s41586-018-0761-3 – ident: e_1_3_2_40_1 doi: 10.1038/s41419-018-1157-x – ident: e_1_3_2_43_1 doi: 10.1096/fj.15-271734 – ident: e_1_3_2_22_1 doi: 10.1038/s41586-018-0372-z – ident: e_1_3_2_31_1 doi: 10.1096/fj.201801585R – ident: e_1_3_2_39_1 doi: 10.4049/jimmunol.1201959 – ident: e_1_3_2_60_1 doi: 10.1161/ATVBAHA.119.313224 – ident: e_1_3_2_4_1 doi: 10.1016/j.redox.2015.01.008 – ident: e_1_3_2_37_1 doi: 10.4049/jimmunol.1900228 – ident: e_1_3_2_12_1 doi: 10.3899/jrheum.180855 – ident: e_1_3_2_26_1 doi: 10.1038/nature11588 – ident: e_1_3_2_63_1 doi: 10.1186/ar3898 – ident: e_1_3_2_46_1 doi: 10.1074/jbc.M112.407130 – ident: e_1_3_2_8_1 doi: 10.1016/j.mrfmmm.2018.09.001 – ident: e_1_3_2_10_1 doi: 10.1007/s10571-020-00855-w – ident: e_1_3_2_44_1 doi: 10.1016/j.biopha.2018.10.129 – ident: e_1_3_2_18_1 doi: 10.4049/jimmunol.1201946 – volume: 49 start-page: 512 year: 2018 ident: e_1_3_2_51_1 article-title: [Soluble uric acid activates NLRP3 inflammasome in myocardial cells through downregulating UCP2]. Sichuan da xue xue bao. Yi xue ban = journal of Sichuan university publication-title: Med Sci Ed – ident: e_1_3_2_11_1 doi: 10.1080/14397595.2020.1740410 – volume: 64 start-page: E107 year: 2018 ident: e_1_3_2_2_1 article-title: Reduction of serum uric acid associated with attenuation of renal injury, inflammation and macrophages M1/M2 ratio in hyperuricemic mice model publication-title: Kobe J Med Sci – ident: e_1_3_2_50_1 doi: 10.1038/srep39884 – ident: e_1_3_2_59_1 doi: 10.1038/s41577-019-0165-0 – ident: e_1_3_2_13_1 doi: 10.1136/annrheumdis-2014-206564 – ident: e_1_3_2_23_1 doi: 10.1159/000345509 – ident: e_1_3_2_30_1 doi: 10.1038/ni.2550 – ident: e_1_3_2_61_1 doi: 10.1016/j.ijbiomac.2020.07.060 – ident: e_1_3_2_54_1 doi: 10.1155/2015/535686 – ident: e_1_3_2_62_1 doi: 10.1038/s12276-019-0254-y – ident: e_1_3_2_32_1 doi: 10.1084/jem.20162040 – ident: e_1_3_2_16_1 doi: 10.12659/MSM.916667 – ident: e_1_3_2_36_1 doi: 10.1016/j.bbamcr.2019.02.007 – ident: e_1_3_2_58_1 doi: 10.1016/j.bcp.2020.113998 – volume: 1 start-page: 13 issue: 3 year: 2019 ident: e_1_3_2_21_1 article-title: The emerging role of mitophagy in kidney diseases publication-title: J Life Sci – ident: e_1_3_2_45_1 doi: 10.1038/ni.1831 – ident: e_1_3_2_25_1 doi: 10.1016/j.immuni.2015.08.008 – ident: e_1_3_2_6_1 doi: 10.3390/cells9020279 – ident: e_1_3_2_28_1 doi: 10.1159/000488048 – ident: e_1_3_2_9_1 doi: 10.3390/antiox9050387 – ident: e_1_3_2_24_1 doi: 10.4049/jimmunol.1701723 – ident: e_1_3_2_41_1 doi: 10.3892/ijmm.2015.2148 – ident: e_1_3_2_48_1 doi: 10.1002/jcb.26806 – ident: e_1_3_2_42_1 doi: 10.1155/2017/8316560 – ident: e_1_3_2_49_1 doi: 10.1155/2018/7635274 – ident: e_1_3_2_20_1 doi: 10.1016/j.freeradbiomed.2018.08.011 – ident: e_1_3_2_52_1 doi: 10.1074/jbc.M113.470971 – ident: e_1_3_2_14_1 doi: 10.3389/fcell.2020.00167 – ident: e_1_3_2_55_1 doi: 10.1080/0886022X.2019.1633350 – ident: e_1_3_2_56_1 doi: 10.1016/j.bbrc.2019.02.141 – ident: e_1_3_2_47_1 doi: 10.1038/s41598-019-42130-z – ident: e_1_3_2_15_1 doi: 10.1002/bab.1700 – ident: e_1_3_2_5_1 doi: 10.1186/s12882-019-1506-8 – ident: e_1_3_2_57_1 doi: 10.1016/j.bbrc.2017.02.019 – ident: e_1_3_2_34_1 doi: 10.1074/mcp.M112.024661 – ident: e_1_3_2_53_1 doi: 10.1007/s12020-014-0239-5 – ident: e_1_3_2_35_1 doi: 10.3389/fimmu.2018.00316 – ident: e_1_3_2_38_1 doi: 10.1007/s10157-019-01705-w – ident: e_1_3_2_3_1 doi: 10.1016/j.phymed.2019.153111 – ident: e_1_3_2_7_1 doi: 10.1159/000484274 – ident: e_1_3_2_17_1 doi: 10.1016/j.cell.2015.12.057 – ident: e_1_3_2_27_1 doi: 10.1083/jcb.201709057
SSID	ssj0015872
Score	2.5439253
SecondaryResourceType	review_article
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...
SourceID	doaj pubmedcentral proquest pubmed crossref informaworld
SourceType	Open Website Open Access Repository Aggregation Database Index Database Enrichment Source Publisher
StartPage	615
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
SummonAdditionalLinks	– databaseName: ProQuest Central dbid: BENPR link: http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV1Lb9QwELZgixAX3tBAQUbiGkhix4lPiKJWHMpqVYG0N8vxo0R0k7LZVuLfM5M4YbdC9MAxiS15NOPxxDPzfYS8RR5ArWUaCy1YDDvRxZVPqjj3YC3el7ocNH1SzOflcikX4cKtC2WVo0_sHbVtDd6Rv88KmJUUmcg_XPyMkTUKs6uBQuM22UOkMj4je4dH88XplEfIy56-CbYSltpmy7GHB9G1S6Rfypbwj5hhRxYTAkm_t06nHsT_GoTp3wLR6_WUWwfU8YP_Fe0huR9CU_pxsKVH5JZrHpO7X0Ly_Qk5H6v0aF_UBS6Stg3tm2GcpSuHPcR1t4K3niJWEdWmthQbJ_Datzmj85PTBaMgJ1jhSnftysEDNQM8L_1R28b9oiFj9JR8Oz76-ulzHMgaYgMh1Ca23mYV44VwuYV_FmdBIK25kUzknhXem7Rwhmfaeq4h6mG80lJDvClyZwvm2DMya9rG7RPKEeMuqeAUYY6XiZFlbo2pdCm1rUzlI8JHJSkTkMyRUONcpSPgadCtQt2qoNuIvJumXQxQHjdNOEQLmAYjEnf_ol2fqbCxVVUJC1GaloYl3HqJzVMJh4WnjjtRphGR2_ajNv1FjB9YUxS7YQEHo8Go4Fo69cdaIvJm-gxOATM9unHtJYwRoAhQi-QReT7Y5iQFgyMuE6WMSLFjtTti7n5p6u898LjsAfiLF_9e1ktyD4UYan4OyGyzvnSvyB1ztam79euwQ38D1lVBZQ priority: 102 providerName: ProQuest – databaseName: Taylor & Francis Journals Complete dbid: TFW link: http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1Lb9QwELZQhRAX3o9AQUbiGkhix4mPgFhxKKsKFbE3y8-yajdBmy0S_54Zx4m6FagHOMaPyGPPeMb2zDeEvMY8gFrLMhdasBwk0ecmFCavA3BLCK1ux5U-apbLdrWSx8mbcEhulXiGDiNQRNyrUbi1GSaPuLcgGAJUzwpOdxXGUjEhKjy1g-rHHAYni2_zO0LdxvRN2CPHLlMMz9_-sqedIoj_FQjTPxmiV_0pLymoxd3_QNo9cidZp_TdyE73yQ3fPSC3Pqf394fkfHLUo9GvC3ZJ2nc0xsN4Rzcew4jXwwZKA0W4Iqrt2lGMncCb3-6ULo--HDMKpAIjbvTQbzx8UDsi9NKztev8L5oejR6Rr4uPJx8-5SlfQ27BitrlLrjKMN4IXzs4tnhXNJXW3Eom6sCaEGzZeMsr7QLXYPgwbrTUYHKK2ruGefaYHHR9558SyhHmrjCgSJjnbWFlWztrjW6ldsaakBE-rZOyCcwcc2qcq3LCPE0zqXAmVZrJjLyZu_0Y0Tyu6_AemWBujGDcsaDfnqok28oY4cBQ09KygrsgMX6q4DDw0nMv2jIj8jILqV28iwlj4hTFrhnA4cRvKu0ug6oakCCYXFFn5NVcDfsCPvbozvcX0EbAQsCySJ6RJyN7zlQw0HKVaGVGmj3G3SNzv6Zbf4_Y4zJi8DfP_oGk5-Q2fo4-QYfkYLe98C_ITftztx62L6P8_gYGokKD priority: 102 providerName: Taylor & Francis
Title	Research progress on related mechanisms of uric acid activating NLRP3 inflammasome in chronic kidney disease
URI	https://www.tandfonline.com/doi/abs/10.1080/0886022X.2022.2036620 https://www.ncbi.nlm.nih.gov/pubmed/35382689 https://www.proquest.com/docview/2780607265 https://www.proquest.com/docview/2647656294 https://pubmed.ncbi.nlm.nih.gov/PMC9004527 https://doaj.org/article/bb6d710a9c304df9b6fc043e41e4e681
Volume	44
WOSCitedRecordID	wos000779448300001&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
hasFullText	1
inHoldings	1
isFullTextHit
isPrint
journalDatabaseRights	– providerCode: PRVAON databaseName: DOAJ Directory of Open Access Journals customDbUrl: eissn: 1525-6049 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0015872 issn: 0886-022X databaseCode: DOA dateStart: 20160101 isFulltext: true titleUrlDefault: https://www.doaj.org/ providerName: Directory of Open Access Journals – providerCode: PRVPQU databaseName: ProQuest Central customDbUrl: eissn: 1525-6049 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0015872 issn: 0886-022X databaseCode: BENPR dateStart: 20171101 isFulltext: true titleUrlDefault: https://www.proquest.com/central providerName: ProQuest – providerCode: PRVPQU databaseName: ProQuest Health & Medical Collection customDbUrl: eissn: 1525-6049 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0015872 issn: 0886-022X databaseCode: 7X7 dateStart: 20171101 isFulltext: true titleUrlDefault: https://search.proquest.com/healthcomplete providerName: ProQuest – providerCode: PRVPQU databaseName: Publicly Available Content Database customDbUrl: eissn: 1525-6049 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0015872 issn: 0886-022X databaseCode: PIMPY dateStart: 20171101 isFulltext: true titleUrlDefault: http://search.proquest.com/publiccontent providerName: ProQuest – providerCode: PRVPQU databaseName: Research Library customDbUrl: eissn: 1525-6049 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0015872 issn: 0886-022X databaseCode: M2O dateStart: 20171101 isFulltext: true titleUrlDefault: https://search.proquest.com/pqrl providerName: ProQuest – providerCode: PRVAWR databaseName: Taylor & Francis Journals Complete customDbUrl: eissn: 1525-6049 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0015872 issn: 0886-022X databaseCode: TFW dateStart: 20170101 isFulltext: true titleUrlDefault: https://www.tandfonline.com providerName: Taylor & Francis – providerCode: PRVAWR databaseName: Taylor & Francis Open Access customDbUrl: eissn: 1525-6049 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0015872 issn: 0886-022X databaseCode: 0YH dateStart: 19870101 isFulltext: true titleUrlDefault: https://www.tandfonline.com providerName: Taylor & Francis
link	http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1bb9MwFLZgIMQL4k5gVEbiNZDaji-PDK0a0lqiaYjuKfJ1RKwpWjsk_j3HTlK1E1JfeLEUJ5Fif5_t4_ic7yD0PuYB1FqNc645zWEk-tyEwuRlALaEILXskD4Vs5mcz1W1leor-oR18sBdx300hjtYBbWysPF2QcXglIJRz8aeeZ6CrglYPcNmqj8_KGVK2wRDKLrYkvkQuxNVtWVMu0TmsDckMRKLch6TfW-tSkm8_5Z06b8M0Nt-lFsL0-QxetRblPhT15In6I5vn6IH0_7M_Bm6GpzrcPLFgpkNL1ucYli8wwsfQ3-b1QJqA44SQ1jbxuEY7xD_1raXeHZ6VlEMnwnkWejVcuHhAttOVRf_bFzr_-D-oOc5-jY5Pv98kvc5FnILls86d8ERQ5ngvnSw1fCuEERrZhXlZaAiBDsW3jKiXWAajBXKjFYazEReeieopy_QQbts_SuEWZSmKwxM_oCOLKySpbPWaKm0M9aEDLGhj2vbC5DHPBhX9XjQKe2hqSM0dQ9Nhj5sXvvVKXDse-EoArh5OApopwqgVd3Tqt5Hqwypbfjrdfp_ErpkJzXd8wGHA1fqfkZY1UQA66FzeZmhd5vbMJbjAY1u_fIGnuEABMCiWIZedtTatILCykS4VBkSO6Tbaebunbb5kfTCVdLNF6__R7-8QQ9jUzuHnkN0sL6-8W_Rfft73ayuR-hucXECpZiLVMoRund0PKvORml4QjklX6Gu-jKtLuDqfPL9L2lDOnQ
linkProvider	Directory of Open Access Journals
linkToHtml	http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMw1V1Jb9QwFLZKQcCFfQkUMBIcA0ns2PEBIbaqVaejChVpbq7jpYzoJGVmCuqf4jfyXpZhpkL01APHLI7s-HuL7ffeR8gL5AE0RqWxMILFIIk-LkNSxnkAtIRQmKKd6YEcDovRSO2tkV99LgyGVfY6sVHUrra4R_46k9AqkZnI3x5_j5E1Ck9XewqNFhY7_vQnLNlmb7Y_wvy-zLLNT_sftuKOVSC2YOvnsQsuKxmXwucOnGvv4KPGcKuYyAOTIdhUessz4wI3YJ4ZL40y4BiJ3DvJPIPvXiKXQY9LDCGTo8UCL82LhiwKBBcDe7NRnzGEtbwLJHvKRrAizTD_iwmBFONLtrChDDhTMPVvbu_Z6M0lc7h583_7kbfIjc7xpu9aSblN1nx1h1zd7UIL7pKjPgaRNiFrYABoXdEm1cc7OvGYIT2eTeBuoFiJiRo7dhTTQnBTuzqkw8HnPUbhv4KMTcysnni4oLYtPky_jV3lT2l3HnaPfLmQsd4n61Vd-YeEcqzgl5RgI5nnRWJVkTtrS1Mo40pbhojwHhTadnXakS7kSKd9OdcOSxqxpDssReTVotlxW6jkvAbvEXGLl7HOeHOjnh7qTm3pshQOfFCjLEu4CwpTwxIOHU8996JII6KW8arnzTZTaDlhNDunAxs9QHWnOGf6Dzoj8nzxGFQenmOZytcn8I6AiYBpUTwiD1pZWIyCgQHPRKEiIlekZGWYq0-q8demrLpq6AXko3936xm5trW_O9CD7eHOY3IdB9RGN22Q9fn0xD8hV-yP-Xg2fdroBkoOLlqGfgMiJJ5b
linkToPdf	http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1Lb9QwELZQQRWX8oZAASNxDSSx48RHXisQy2qFitib5WeJ6CbVZluJf8_YcaJuBeoBjrHjyGPPeGbimW8QeunrAErJ85RJRlKQRJsql6m0dMAtztWyHnZ6Xi0W9WrFlzGasI9hld6HdgNQRDirvXCfGjdGxL0GwWCgelbg3RU-l4owVoDXfh1MZ-b9r6PZ9-kioaxD_SY_JPVjxiSev31mRz0FFP9LGKZ_skQvB1Re0FCzW_-BttvoIJqn-M3AT3fQNdveRftf4gX8PXQyRurhENgFxyTuWhwSYqzBa-vziJt-Da0Oe7wiLHVjsE-e8L9-22O8mH9dEgykAieuZd-tLTxgPUD04p-Nae0vHG-N7qNvsw9H7z6msWBDqsGM2qbGmUIRWjFbGvBbrMmqQkqqOWGlI5VzOq-spoU0jkqwfAhVkkuwOVlpTUUseYD22q61jxCmHucuU6BJiKV1pnldGq2VrLk0SiuXIDruk9ARzdwX1TgR-Qh6GldS-JUUcSUT9GoadjrAeVw14K1ngullj8YdGrrNsYjCLZRiBiw1yTXJqHHcJ1BlFCaeW2pZnSeIX2QhsQ0_Y9xQOUWQKyZwOPKbiMdLL4oKRAgWl5UJejF1w8Hgb3tka7szeIfBRsC2cJqghwN7TlQQUHMFq3mCqh3G3SFzt6dtfgTwcR5A-KvH_0DSc7S_fD8T80-Lz0_QTd8zxAcdor3t5sw-RTf0-bbpN8-CKP8GPCdFXw
openUrl	ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Research+progress+on+related+mechanisms+of+uric+acid+activating+NLRP3+inflammasome+in+chronic+kidney+disease&rft.jtitle=Renal+failure&rft.au=Wang%2C+Miao&rft.au=Lin%2C+Xin&rft.au=Yang%2C+Xiaoming&rft.au=Yang%2C+Yanlang&rft.date=2022-12-01&rft.eissn=1525-6049&rft.volume=44&rft.issue=1&rft.spage=615&rft_id=info:doi/10.1080%2F0886022X.2022.2036620&rft_id=info%3Apmid%2F35382689&rft.externalDocID=35382689
thumbnail_l	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0886-022X&client=summon
thumbnail_m	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0886-022X&client=summon
thumbnail_s	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0886-022X&client=summon