MiR‐223‐3p and miR‐22‐3p inhibit monosodium urate‐induced gouty inflammation by targeting NLRP3
Background MicroRNAs (miRNAs) have been shown to play a crucial role in inflammation regulation; however, their relationship with inflammation in acute gouty arthritis has not been fully elucidated. Herein, we conducted a study to explore the regulatory roles of miR‐223‐3p and miR‐22‐3p in gouty‐ass...
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| Veröffentlicht in: | International journal of rheumatic diseases 2021-04, Vol.24 (4), p.599-607 |
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| creator | Wang, Xiang Chi, Jingwei Dong, Bingzi Xu, Lili Zhou, Yue Huang, Yajing Sun, Shengnan Wei, Fanxiang Liu, Yuzhao Liu, Chuanfeng Che, Kui Lv, Wenshan Chen, Ying Wang, Yangang |
| description | Background
MicroRNAs (miRNAs) have been shown to play a crucial role in inflammation regulation; however, their relationship with inflammation in acute gouty arthritis has not been fully elucidated. Herein, we conducted a study to explore the regulatory roles of miR‐223‐3p and miR‐22‐3p in gouty‐associated inflammation.
Methods
In vitro and in vivo experiments were conducted to examine the molecular mechanisms of miRNA regulation in gouty inflammation. Dual‐luciferase reporter assay was used to verify the direct target of miR‐223‐3p and miR‐22‐3p.
Results
We found that miR‐223‐3p and miR‐22‐3p interacted with the 3′ untranslated region segment of NLRP3 (nucleotide‐binding domain leucine‐rich repeat [NLR] and pyrin domain containing receptor 3) and inhibited its expression. A decreased expression of miR‐223‐3p and miR‐22‐3p was observed in both mice air pouch synovium and phorbol myristrate acetate‐treated THP‐1 cells stimulated with monosodium urate (P |
| doi_str_mv | 10.1111/1756-185X.14089 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_2509218517</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2509218517</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3719-90b50a1805d9c6e91bcf05e753a23fdd0bc55838f73649e252575bba5c272dca3</originalsourceid><addsrcrecordid>eNqFkE1LwzAch4MoTqdnbxLw3C0vS9Mex_ANqo6h4C3krTNjbWfaIr35EfyMfhIzO3c1hyT88vx_gQeAC4xGOKwx5iyOcMJeR3iCkvQAnOyTw_19ggfgtK5XCMWYxvwYDCiNGaI4OQHuwS2-P78IoWGnGyhLA4td1CeufHPKNbCoyqqujGsL2HrZ2PDqStNqa-CyapsugPlaFoVsXFVC1cFG-qVtXLmEj9liTs_AUS7XtT3fnUPwcnP9PLuLsqfb-9k0izTlOI1SpBiSOEHMpDq2KVY6R8xyRiWhuTFIacYSmuScxpPUEkYYZ0pJpgknRks6BFd978ZX762tG7GqWl-GLwVhKCXBDeaBGveU9lVde5uLjXeF9J3ASGzViq08sRUpftWGictdb6sKa_b8n8sAsB74cGvb_dcnpvOsL_4BhjiGyw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2509218517</pqid></control><display><type>article</type><title>MiR‐223‐3p and miR‐22‐3p inhibit monosodium urate‐induced gouty inflammation by targeting NLRP3</title><source>MEDLINE</source><source>Access via Wiley Online Library</source><creator>Wang, Xiang ; Chi, Jingwei ; Dong, Bingzi ; Xu, Lili ; Zhou, Yue ; Huang, Yajing ; Sun, Shengnan ; Wei, Fanxiang ; Liu, Yuzhao ; Liu, Chuanfeng ; Che, Kui ; Lv, Wenshan ; Chen, Ying ; Wang, Yangang</creator><creatorcontrib>Wang, Xiang ; Chi, Jingwei ; Dong, Bingzi ; Xu, Lili ; Zhou, Yue ; Huang, Yajing ; Sun, Shengnan ; Wei, Fanxiang ; Liu, Yuzhao ; Liu, Chuanfeng ; Che, Kui ; Lv, Wenshan ; Chen, Ying ; Wang, Yangang</creatorcontrib><description>Background
MicroRNAs (miRNAs) have been shown to play a crucial role in inflammation regulation; however, their relationship with inflammation in acute gouty arthritis has not been fully elucidated. Herein, we conducted a study to explore the regulatory roles of miR‐223‐3p and miR‐22‐3p in gouty‐associated inflammation.
Methods
In vitro and in vivo experiments were conducted to examine the molecular mechanisms of miRNA regulation in gouty inflammation. Dual‐luciferase reporter assay was used to verify the direct target of miR‐223‐3p and miR‐22‐3p.
Results
We found that miR‐223‐3p and miR‐22‐3p interacted with the 3′ untranslated region segment of NLRP3 (nucleotide‐binding domain leucine‐rich repeat [NLR] and pyrin domain containing receptor 3) and inhibited its expression. A decreased expression of miR‐223‐3p and miR‐22‐3p was observed in both mice air pouch synovium and phorbol myristrate acetate‐treated THP‐1 cells stimulated with monosodium urate (P < .05). Compared with the negative control group, NLRP3 expression at the transcript and protein level in miR‐223‐3p and miR‐22‐3p overexpression group significantly decreased after 6 hours of monosodium urate treatment in vivo and in vitro (P < .05). The results of the dual‐luciferase reporter assay demonstrated that miR‐223‐3p and miR‐22‐3p directly targeted NLRP3.
Conclusion
The findings of the present study show that miR‐223‐3p and miR‐22‐3p can reduce the inflammatory effects of gout by inhibiting the expression of NLRP3.</description><identifier>ISSN: 1756-1841</identifier><identifier>EISSN: 1756-185X</identifier><identifier>DOI: 10.1111/1756-185X.14089</identifier><identifier>PMID: 33650318</identifier><language>eng</language><publisher>England: Wiley Subscription Services, Inc</publisher><subject>3' Untranslated Regions ; Acetic acid ; Animals ; Arthritis ; Arthritis, Gouty - chemically induced ; Arthritis, Gouty - immunology ; Arthritis, Gouty - metabolism ; Arthritis, Gouty - prevention & control ; Binding Sites ; Disease Models, Animal ; Down-Regulation ; Gout ; gouty inflammation ; Humans ; Inflammasomes - genetics ; Inflammasomes - metabolism ; Inflammation ; Inflammation - chemically induced ; Inflammation - immunology ; Inflammation - metabolism ; Inflammation - prevention & control ; Leucine ; Male ; Mice ; Mice, Inbred BALB C ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miRNA ; miR‐223‐3p ; miR‐22‐3p ; Molecular modelling ; monosodium urate ; NLR Family, Pyrin Domain-Containing 3 Protein - genetics ; NLR Family, Pyrin Domain-Containing 3 Protein - metabolism ; NLRP3 ; Pyrin protein ; Signal Transduction ; Synovium ; THP-1 Cells ; Transcription ; Uric Acid</subject><ispartof>International journal of rheumatic diseases, 2021-04, Vol.24 (4), p.599-607</ispartof><rights>2021 Asia Pacific League of Associations for Rheumatology and John Wiley & Sons Australia, Ltd</rights><rights>2021 Asia Pacific League of Associations for Rheumatology and John Wiley & Sons Australia, Ltd.</rights><rights>International Journal of Rheumatic Diseases © 2021 Asia Pacific League of Associations for Rheumatology and John Wiley & Sons Australia, Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3719-90b50a1805d9c6e91bcf05e753a23fdd0bc55838f73649e252575bba5c272dca3</citedby><cites>FETCH-LOGICAL-c3719-90b50a1805d9c6e91bcf05e753a23fdd0bc55838f73649e252575bba5c272dca3</cites><orcidid>0000-0001-6597-420X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2F1756-185X.14089$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2F1756-185X.14089$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33650318$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Xiang</creatorcontrib><creatorcontrib>Chi, Jingwei</creatorcontrib><creatorcontrib>Dong, Bingzi</creatorcontrib><creatorcontrib>Xu, Lili</creatorcontrib><creatorcontrib>Zhou, Yue</creatorcontrib><creatorcontrib>Huang, Yajing</creatorcontrib><creatorcontrib>Sun, Shengnan</creatorcontrib><creatorcontrib>Wei, Fanxiang</creatorcontrib><creatorcontrib>Liu, Yuzhao</creatorcontrib><creatorcontrib>Liu, Chuanfeng</creatorcontrib><creatorcontrib>Che, Kui</creatorcontrib><creatorcontrib>Lv, Wenshan</creatorcontrib><creatorcontrib>Chen, Ying</creatorcontrib><creatorcontrib>Wang, Yangang</creatorcontrib><title>MiR‐223‐3p and miR‐22‐3p inhibit monosodium urate‐induced gouty inflammation by targeting NLRP3</title><title>International journal of rheumatic diseases</title><addtitle>Int J Rheum Dis</addtitle><description>Background
MicroRNAs (miRNAs) have been shown to play a crucial role in inflammation regulation; however, their relationship with inflammation in acute gouty arthritis has not been fully elucidated. Herein, we conducted a study to explore the regulatory roles of miR‐223‐3p and miR‐22‐3p in gouty‐associated inflammation.
Methods
In vitro and in vivo experiments were conducted to examine the molecular mechanisms of miRNA regulation in gouty inflammation. Dual‐luciferase reporter assay was used to verify the direct target of miR‐223‐3p and miR‐22‐3p.
Results
We found that miR‐223‐3p and miR‐22‐3p interacted with the 3′ untranslated region segment of NLRP3 (nucleotide‐binding domain leucine‐rich repeat [NLR] and pyrin domain containing receptor 3) and inhibited its expression. A decreased expression of miR‐223‐3p and miR‐22‐3p was observed in both mice air pouch synovium and phorbol myristrate acetate‐treated THP‐1 cells stimulated with monosodium urate (P < .05). Compared with the negative control group, NLRP3 expression at the transcript and protein level in miR‐223‐3p and miR‐22‐3p overexpression group significantly decreased after 6 hours of monosodium urate treatment in vivo and in vitro (P < .05). The results of the dual‐luciferase reporter assay demonstrated that miR‐223‐3p and miR‐22‐3p directly targeted NLRP3.
Conclusion
The findings of the present study show that miR‐223‐3p and miR‐22‐3p can reduce the inflammatory effects of gout by inhibiting the expression of NLRP3.</description><subject>3' Untranslated Regions</subject><subject>Acetic acid</subject><subject>Animals</subject><subject>Arthritis</subject><subject>Arthritis, Gouty - chemically induced</subject><subject>Arthritis, Gouty - immunology</subject><subject>Arthritis, Gouty - metabolism</subject><subject>Arthritis, Gouty - prevention & control</subject><subject>Binding Sites</subject><subject>Disease Models, Animal</subject><subject>Down-Regulation</subject><subject>Gout</subject><subject>gouty inflammation</subject><subject>Humans</subject><subject>Inflammasomes - genetics</subject><subject>Inflammasomes - metabolism</subject><subject>Inflammation</subject><subject>Inflammation - chemically induced</subject><subject>Inflammation - immunology</subject><subject>Inflammation - metabolism</subject><subject>Inflammation - prevention & control</subject><subject>Leucine</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>miR‐223‐3p</subject><subject>miR‐22‐3p</subject><subject>Molecular modelling</subject><subject>monosodium urate</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein - genetics</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</subject><subject>NLRP3</subject><subject>Pyrin protein</subject><subject>Signal Transduction</subject><subject>Synovium</subject><subject>THP-1 Cells</subject><subject>Transcription</subject><subject>Uric Acid</subject><issn>1756-1841</issn><issn>1756-185X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1LwzAch4MoTqdnbxLw3C0vS9Mex_ANqo6h4C3krTNjbWfaIr35EfyMfhIzO3c1hyT88vx_gQeAC4xGOKwx5iyOcMJeR3iCkvQAnOyTw_19ggfgtK5XCMWYxvwYDCiNGaI4OQHuwS2-P78IoWGnGyhLA4td1CeufHPKNbCoyqqujGsL2HrZ2PDqStNqa-CyapsugPlaFoVsXFVC1cFG-qVtXLmEj9liTs_AUS7XtT3fnUPwcnP9PLuLsqfb-9k0izTlOI1SpBiSOEHMpDq2KVY6R8xyRiWhuTFIacYSmuScxpPUEkYYZ0pJpgknRks6BFd978ZX762tG7GqWl-GLwVhKCXBDeaBGveU9lVde5uLjXeF9J3ASGzViq08sRUpftWGictdb6sKa_b8n8sAsB74cGvb_dcnpvOsL_4BhjiGyw</recordid><startdate>202104</startdate><enddate>202104</enddate><creator>Wang, Xiang</creator><creator>Chi, Jingwei</creator><creator>Dong, Bingzi</creator><creator>Xu, Lili</creator><creator>Zhou, Yue</creator><creator>Huang, Yajing</creator><creator>Sun, Shengnan</creator><creator>Wei, Fanxiang</creator><creator>Liu, Yuzhao</creator><creator>Liu, Chuanfeng</creator><creator>Che, Kui</creator><creator>Lv, Wenshan</creator><creator>Chen, Ying</creator><creator>Wang, Yangang</creator><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7T5</scope><scope>H94</scope><orcidid>https://orcid.org/0000-0001-6597-420X</orcidid></search><sort><creationdate>202104</creationdate><title>MiR‐223‐3p and miR‐22‐3p inhibit monosodium urate‐induced gouty inflammation by targeting NLRP3</title><author>Wang, Xiang ; Chi, Jingwei ; Dong, Bingzi ; Xu, Lili ; Zhou, Yue ; Huang, Yajing ; Sun, Shengnan ; Wei, Fanxiang ; Liu, Yuzhao ; Liu, Chuanfeng ; Che, Kui ; Lv, Wenshan ; Chen, Ying ; Wang, Yangang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3719-90b50a1805d9c6e91bcf05e753a23fdd0bc55838f73649e252575bba5c272dca3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>3' Untranslated Regions</topic><topic>Acetic acid</topic><topic>Animals</topic><topic>Arthritis</topic><topic>Arthritis, Gouty - chemically induced</topic><topic>Arthritis, Gouty - immunology</topic><topic>Arthritis, Gouty - metabolism</topic><topic>Arthritis, Gouty - prevention & control</topic><topic>Binding Sites</topic><topic>Disease Models, Animal</topic><topic>Down-Regulation</topic><topic>Gout</topic><topic>gouty inflammation</topic><topic>Humans</topic><topic>Inflammasomes - genetics</topic><topic>Inflammasomes - metabolism</topic><topic>Inflammation</topic><topic>Inflammation - chemically induced</topic><topic>Inflammation - immunology</topic><topic>Inflammation - metabolism</topic><topic>Inflammation - prevention & control</topic><topic>Leucine</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miRNA</topic><topic>miR‐223‐3p</topic><topic>miR‐22‐3p</topic><topic>Molecular modelling</topic><topic>monosodium urate</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein - genetics</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</topic><topic>NLRP3</topic><topic>Pyrin protein</topic><topic>Signal Transduction</topic><topic>Synovium</topic><topic>THP-1 Cells</topic><topic>Transcription</topic><topic>Uric Acid</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Xiang</creatorcontrib><creatorcontrib>Chi, Jingwei</creatorcontrib><creatorcontrib>Dong, Bingzi</creatorcontrib><creatorcontrib>Xu, Lili</creatorcontrib><creatorcontrib>Zhou, Yue</creatorcontrib><creatorcontrib>Huang, Yajing</creatorcontrib><creatorcontrib>Sun, Shengnan</creatorcontrib><creatorcontrib>Wei, Fanxiang</creatorcontrib><creatorcontrib>Liu, Yuzhao</creatorcontrib><creatorcontrib>Liu, Chuanfeng</creatorcontrib><creatorcontrib>Che, Kui</creatorcontrib><creatorcontrib>Lv, Wenshan</creatorcontrib><creatorcontrib>Chen, Ying</creatorcontrib><creatorcontrib>Wang, Yangang</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>International journal of rheumatic diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Xiang</au><au>Chi, Jingwei</au><au>Dong, Bingzi</au><au>Xu, Lili</au><au>Zhou, Yue</au><au>Huang, Yajing</au><au>Sun, Shengnan</au><au>Wei, Fanxiang</au><au>Liu, Yuzhao</au><au>Liu, Chuanfeng</au><au>Che, Kui</au><au>Lv, Wenshan</au><au>Chen, Ying</au><au>Wang, Yangang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MiR‐223‐3p and miR‐22‐3p inhibit monosodium urate‐induced gouty inflammation by targeting NLRP3</atitle><jtitle>International journal of rheumatic diseases</jtitle><addtitle>Int J Rheum Dis</addtitle><date>2021-04</date><risdate>2021</risdate><volume>24</volume><issue>4</issue><spage>599</spage><epage>607</epage><pages>599-607</pages><issn>1756-1841</issn><eissn>1756-185X</eissn><abstract>Background
MicroRNAs (miRNAs) have been shown to play a crucial role in inflammation regulation; however, their relationship with inflammation in acute gouty arthritis has not been fully elucidated. Herein, we conducted a study to explore the regulatory roles of miR‐223‐3p and miR‐22‐3p in gouty‐associated inflammation.
Methods
In vitro and in vivo experiments were conducted to examine the molecular mechanisms of miRNA regulation in gouty inflammation. Dual‐luciferase reporter assay was used to verify the direct target of miR‐223‐3p and miR‐22‐3p.
Results
We found that miR‐223‐3p and miR‐22‐3p interacted with the 3′ untranslated region segment of NLRP3 (nucleotide‐binding domain leucine‐rich repeat [NLR] and pyrin domain containing receptor 3) and inhibited its expression. A decreased expression of miR‐223‐3p and miR‐22‐3p was observed in both mice air pouch synovium and phorbol myristrate acetate‐treated THP‐1 cells stimulated with monosodium urate (P < .05). Compared with the negative control group, NLRP3 expression at the transcript and protein level in miR‐223‐3p and miR‐22‐3p overexpression group significantly decreased after 6 hours of monosodium urate treatment in vivo and in vitro (P < .05). The results of the dual‐luciferase reporter assay demonstrated that miR‐223‐3p and miR‐22‐3p directly targeted NLRP3.
Conclusion
The findings of the present study show that miR‐223‐3p and miR‐22‐3p can reduce the inflammatory effects of gout by inhibiting the expression of NLRP3.</abstract><cop>England</cop><pub>Wiley Subscription Services, Inc</pub><pmid>33650318</pmid><doi>10.1111/1756-185X.14089</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0001-6597-420X</orcidid></addata></record> |
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| subjects | 3' Untranslated Regions Acetic acid Animals Arthritis Arthritis, Gouty - chemically induced Arthritis, Gouty - immunology Arthritis, Gouty - metabolism Arthritis, Gouty - prevention & control Binding Sites Disease Models, Animal Down-Regulation Gout gouty inflammation Humans Inflammasomes - genetics Inflammasomes - metabolism Inflammation Inflammation - chemically induced Inflammation - immunology Inflammation - metabolism Inflammation - prevention & control Leucine Male Mice Mice, Inbred BALB C MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism miRNA miR‐223‐3p miR‐22‐3p Molecular modelling monosodium urate NLR Family, Pyrin Domain-Containing 3 Protein - genetics NLR Family, Pyrin Domain-Containing 3 Protein - metabolism NLRP3 Pyrin protein Signal Transduction Synovium THP-1 Cells Transcription Uric Acid |
| title | MiR‐223‐3p and miR‐22‐3p inhibit monosodium urate‐induced gouty inflammation by targeting NLRP3 |
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