LncRNA H19 Mitigates Oxidized Low-Density Lipoprotein Induced Pyroptosis via Caspase-1 in Raw 264.7 Cells
Atherosclerosis (AS) is mainly characterized by the activation of inflammatory cells and chronic inflammatory responses after cell injury. Pyroptosis is a form of programmed cell death (PCD) accompanied by the release of inflammatory factors. Many studies have shown that pyroptosis plays an importan...
Gespeichert in:
| Veröffentlicht in: | Inflammation 2021-12, Vol.44 (6), p.2407-2418 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 2418 |
|---|---|
| container_issue | 6 |
| container_start_page | 2407 |
| container_title | Inflammation |
| container_volume | 44 |
| creator | Liu, Shan Xu, Dong-sheng Ma, Jiu-long Huang, Peng Wu, Di Ren, Li-qun |
| description | Atherosclerosis (AS) is mainly characterized by the activation of inflammatory cells and chronic inflammatory responses after cell injury. Pyroptosis is a form of programmed cell death (PCD) accompanied by the release of inflammatory factors. Many studies have shown that pyroptosis plays an important role in AS. Increasing evidence also indicates that long non-coding RNA H19 (lncRNA H19) involved in AS. However, whether the role of lncRNA H19 in AS is related to pyroptosis and the underlying mechanisms are largely unknown. In this study, we found that oxidized low-density lipoprotein (ox-LDL) induced pyroptosis and decreased the expression of lncRNA H19 in Raw 264.7 cells. Besides, silencing endogenous lncRNA H19 increased inflammatory responses and pyroptosis while exogenous overexpression of lncRNA H19 reversed this effect. Notably, we identified that the inhibitor of caspase-1 (XV-765) completely abrogated the silencing endogenous lncRNA H19 mediated pyroptosis. In addition, we found that lncRNA H19 inhibited ox-LDL-induced activation of nuclear factor-kappa B (NF-κB), mitochondrial dysfunction, and reduced the production of reactive oxygen species (ROS). Moreover, VX-765 impaired the silencing endogenous lncRNA H19 mediated pyroptosis. Overall, these findings indicated that lncRNA H19 may play an important role in pyroptosis and may serve as a potential therapeutic target for AS. |
| doi_str_mv | 10.1007/s10753-021-01511-1 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_2602328372</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2602328372</sourcerecordid><originalsourceid>FETCH-LOGICAL-c375t-f76de954748c7ba66c0773476817ad6fd3311fa968444ec5c1e5e7318f51390c3</originalsourceid><addsrcrecordid>eNp9kMtOwzAQRS0EgvL4ARbIEmuDJ-NHskTlUaRAEYK1ZRwHGZUkxCmlfD2G8tixmsWce2d0CNkHfgSc6-MIXEtkPAPGQQIwWCMjkBpZJrVaJyOOijMsCr1FtmN84pznRY6bZAsFCiiAj0goG3d7fUInUNCrMIRHO_hIp2-hCu--omW7YKe-iWFY0jJ0bde3gw8NvWyquUv7m2XfdkMbQ6SvwdKxjZ2NngFNzK1d0EyJI03HfjaLu2SjtrPo977nDrk_P7sbT1g5vbgcn5TMoZYDq7WqfCGFFrnTD1Ypx7VGoVUO2laqrhABaluoXAjhnXTgpdcIeS0BC-5whxyuetOvL3MfB_PUzvsmnTSZ4hlmOeosUdmKcn0bY-9r0_Xh2fZLA9x82jUruybZNV92DaTQwXf1_OHZV7-RH50JwBUQ06p59P3f7X9qPwAgv4Ib</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2602328372</pqid></control><display><type>article</type><title>LncRNA H19 Mitigates Oxidized Low-Density Lipoprotein Induced Pyroptosis via Caspase-1 in Raw 264.7 Cells</title><source>MEDLINE</source><source>SpringerNature Journals</source><creator>Liu, Shan ; Xu, Dong-sheng ; Ma, Jiu-long ; Huang, Peng ; Wu, Di ; Ren, Li-qun</creator><creatorcontrib>Liu, Shan ; Xu, Dong-sheng ; Ma, Jiu-long ; Huang, Peng ; Wu, Di ; Ren, Li-qun</creatorcontrib><description>Atherosclerosis (AS) is mainly characterized by the activation of inflammatory cells and chronic inflammatory responses after cell injury. Pyroptosis is a form of programmed cell death (PCD) accompanied by the release of inflammatory factors. Many studies have shown that pyroptosis plays an important role in AS. Increasing evidence also indicates that long non-coding RNA H19 (lncRNA H19) involved in AS. However, whether the role of lncRNA H19 in AS is related to pyroptosis and the underlying mechanisms are largely unknown. In this study, we found that oxidized low-density lipoprotein (ox-LDL) induced pyroptosis and decreased the expression of lncRNA H19 in Raw 264.7 cells. Besides, silencing endogenous lncRNA H19 increased inflammatory responses and pyroptosis while exogenous overexpression of lncRNA H19 reversed this effect. Notably, we identified that the inhibitor of caspase-1 (XV-765) completely abrogated the silencing endogenous lncRNA H19 mediated pyroptosis. In addition, we found that lncRNA H19 inhibited ox-LDL-induced activation of nuclear factor-kappa B (NF-κB), mitochondrial dysfunction, and reduced the production of reactive oxygen species (ROS). Moreover, VX-765 impaired the silencing endogenous lncRNA H19 mediated pyroptosis. Overall, these findings indicated that lncRNA H19 may play an important role in pyroptosis and may serve as a potential therapeutic target for AS.</description><identifier>ISSN: 0360-3997</identifier><identifier>EISSN: 1573-2576</identifier><identifier>DOI: 10.1007/s10753-021-01511-1</identifier><identifier>PMID: 34341910</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animals ; Apoptosis ; Arteriosclerosis ; Atherosclerosis ; Atherosclerosis - genetics ; Atherosclerosis - metabolism ; Atherosclerosis - pathology ; Biomedical and Life Sciences ; Biomedicine ; Blood vessels ; Caspase 1 - genetics ; Caspase 1 - metabolism ; Caspase-1 ; Cell activation ; Cell death ; Cell injury ; Chronic illnesses ; Cytokines ; Disease ; Immune system ; Immunology ; Inflammation ; Internal Medicine ; Lipids ; Lipoproteins ; Lipoproteins, LDL - toxicity ; Low density lipoprotein ; Macrophages - drug effects ; Macrophages - metabolism ; Macrophages - pathology ; Mice ; Mitochondria ; Mitochondria - drug effects ; Mitochondria - metabolism ; Mitochondria - pathology ; NF-kappa B - metabolism ; NF-κB protein ; Non-coding RNA ; Original Article ; Pathology ; Pharmacology/Toxicology ; Pyroptosis ; Pyroptosis - drug effects ; RAW 264.7 Cells ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Rheumatology ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; Signal Transduction ; Smooth muscle</subject><ispartof>Inflammation, 2021-12, Vol.44 (6), p.2407-2418</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021</rights><rights>2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-f76de954748c7ba66c0773476817ad6fd3311fa968444ec5c1e5e7318f51390c3</citedby><cites>FETCH-LOGICAL-c375t-f76de954748c7ba66c0773476817ad6fd3311fa968444ec5c1e5e7318f51390c3</cites><orcidid>0000-0003-1503-3721</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10753-021-01511-1$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10753-021-01511-1$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34341910$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Shan</creatorcontrib><creatorcontrib>Xu, Dong-sheng</creatorcontrib><creatorcontrib>Ma, Jiu-long</creatorcontrib><creatorcontrib>Huang, Peng</creatorcontrib><creatorcontrib>Wu, Di</creatorcontrib><creatorcontrib>Ren, Li-qun</creatorcontrib><title>LncRNA H19 Mitigates Oxidized Low-Density Lipoprotein Induced Pyroptosis via Caspase-1 in Raw 264.7 Cells</title><title>Inflammation</title><addtitle>Inflammation</addtitle><addtitle>Inflammation</addtitle><description>Atherosclerosis (AS) is mainly characterized by the activation of inflammatory cells and chronic inflammatory responses after cell injury. Pyroptosis is a form of programmed cell death (PCD) accompanied by the release of inflammatory factors. Many studies have shown that pyroptosis plays an important role in AS. Increasing evidence also indicates that long non-coding RNA H19 (lncRNA H19) involved in AS. However, whether the role of lncRNA H19 in AS is related to pyroptosis and the underlying mechanisms are largely unknown. In this study, we found that oxidized low-density lipoprotein (ox-LDL) induced pyroptosis and decreased the expression of lncRNA H19 in Raw 264.7 cells. Besides, silencing endogenous lncRNA H19 increased inflammatory responses and pyroptosis while exogenous overexpression of lncRNA H19 reversed this effect. Notably, we identified that the inhibitor of caspase-1 (XV-765) completely abrogated the silencing endogenous lncRNA H19 mediated pyroptosis. In addition, we found that lncRNA H19 inhibited ox-LDL-induced activation of nuclear factor-kappa B (NF-κB), mitochondrial dysfunction, and reduced the production of reactive oxygen species (ROS). Moreover, VX-765 impaired the silencing endogenous lncRNA H19 mediated pyroptosis. Overall, these findings indicated that lncRNA H19 may play an important role in pyroptosis and may serve as a potential therapeutic target for AS.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Arteriosclerosis</subject><subject>Atherosclerosis</subject><subject>Atherosclerosis - genetics</subject><subject>Atherosclerosis - metabolism</subject><subject>Atherosclerosis - pathology</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Blood vessels</subject><subject>Caspase 1 - genetics</subject><subject>Caspase 1 - metabolism</subject><subject>Caspase-1</subject><subject>Cell activation</subject><subject>Cell death</subject><subject>Cell injury</subject><subject>Chronic illnesses</subject><subject>Cytokines</subject><subject>Disease</subject><subject>Immune system</subject><subject>Immunology</subject><subject>Inflammation</subject><subject>Internal Medicine</subject><subject>Lipids</subject><subject>Lipoproteins</subject><subject>Lipoproteins, LDL - toxicity</subject><subject>Low density lipoprotein</subject><subject>Macrophages - drug effects</subject><subject>Macrophages - metabolism</subject><subject>Macrophages - pathology</subject><subject>Mice</subject><subject>Mitochondria</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - metabolism</subject><subject>Mitochondria - pathology</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB protein</subject><subject>Non-coding RNA</subject><subject>Original Article</subject><subject>Pathology</subject><subject>Pharmacology/Toxicology</subject><subject>Pyroptosis</subject><subject>Pyroptosis - drug effects</subject><subject>RAW 264.7 Cells</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Rheumatology</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><subject>Signal Transduction</subject><subject>Smooth muscle</subject><issn>0360-3997</issn><issn>1573-2576</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9kMtOwzAQRS0EgvL4ARbIEmuDJ-NHskTlUaRAEYK1ZRwHGZUkxCmlfD2G8tixmsWce2d0CNkHfgSc6-MIXEtkPAPGQQIwWCMjkBpZJrVaJyOOijMsCr1FtmN84pznRY6bZAsFCiiAj0goG3d7fUInUNCrMIRHO_hIp2-hCu--omW7YKe-iWFY0jJ0bde3gw8NvWyquUv7m2XfdkMbQ6SvwdKxjZ2NngFNzK1d0EyJI03HfjaLu2SjtrPo977nDrk_P7sbT1g5vbgcn5TMoZYDq7WqfCGFFrnTD1Ypx7VGoVUO2laqrhABaluoXAjhnXTgpdcIeS0BC-5whxyuetOvL3MfB_PUzvsmnTSZ4hlmOeosUdmKcn0bY-9r0_Xh2fZLA9x82jUruybZNV92DaTQwXf1_OHZV7-RH50JwBUQ06p59P3f7X9qPwAgv4Ib</recordid><startdate>20211201</startdate><enddate>20211201</enddate><creator>Liu, Shan</creator><creator>Xu, Dong-sheng</creator><creator>Ma, Jiu-long</creator><creator>Huang, Peng</creator><creator>Wu, Di</creator><creator>Ren, Li-qun</creator><general>Springer US</general><general>Springer Nature B.V</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>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><orcidid>https://orcid.org/0000-0003-1503-3721</orcidid></search><sort><creationdate>20211201</creationdate><title>LncRNA H19 Mitigates Oxidized Low-Density Lipoprotein Induced Pyroptosis via Caspase-1 in Raw 264.7 Cells</title><author>Liu, Shan ; Xu, Dong-sheng ; Ma, Jiu-long ; Huang, Peng ; Wu, Di ; Ren, Li-qun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-f76de954748c7ba66c0773476817ad6fd3311fa968444ec5c1e5e7318f51390c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Arteriosclerosis</topic><topic>Atherosclerosis</topic><topic>Atherosclerosis - genetics</topic><topic>Atherosclerosis - metabolism</topic><topic>Atherosclerosis - pathology</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Blood vessels</topic><topic>Caspase 1 - genetics</topic><topic>Caspase 1 - metabolism</topic><topic>Caspase-1</topic><topic>Cell activation</topic><topic>Cell death</topic><topic>Cell injury</topic><topic>Chronic illnesses</topic><topic>Cytokines</topic><topic>Disease</topic><topic>Immune system</topic><topic>Immunology</topic><topic>Inflammation</topic><topic>Internal Medicine</topic><topic>Lipids</topic><topic>Lipoproteins</topic><topic>Lipoproteins, LDL - toxicity</topic><topic>Low density lipoprotein</topic><topic>Macrophages - drug effects</topic><topic>Macrophages - metabolism</topic><topic>Macrophages - pathology</topic><topic>Mice</topic><topic>Mitochondria</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - metabolism</topic><topic>Mitochondria - pathology</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB protein</topic><topic>Non-coding RNA</topic><topic>Original Article</topic><topic>Pathology</topic><topic>Pharmacology/Toxicology</topic><topic>Pyroptosis</topic><topic>Pyroptosis - drug effects</topic><topic>RAW 264.7 Cells</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Rheumatology</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>Signal Transduction</topic><topic>Smooth muscle</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Shan</creatorcontrib><creatorcontrib>Xu, Dong-sheng</creatorcontrib><creatorcontrib>Ma, Jiu-long</creatorcontrib><creatorcontrib>Huang, Peng</creatorcontrib><creatorcontrib>Wu, Di</creatorcontrib><creatorcontrib>Ren, Li-qun</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><jtitle>Inflammation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Shan</au><au>Xu, Dong-sheng</au><au>Ma, Jiu-long</au><au>Huang, Peng</au><au>Wu, Di</au><au>Ren, Li-qun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>LncRNA H19 Mitigates Oxidized Low-Density Lipoprotein Induced Pyroptosis via Caspase-1 in Raw 264.7 Cells</atitle><jtitle>Inflammation</jtitle><stitle>Inflammation</stitle><addtitle>Inflammation</addtitle><date>2021-12-01</date><risdate>2021</risdate><volume>44</volume><issue>6</issue><spage>2407</spage><epage>2418</epage><pages>2407-2418</pages><issn>0360-3997</issn><eissn>1573-2576</eissn><abstract>Atherosclerosis (AS) is mainly characterized by the activation of inflammatory cells and chronic inflammatory responses after cell injury. Pyroptosis is a form of programmed cell death (PCD) accompanied by the release of inflammatory factors. Many studies have shown that pyroptosis plays an important role in AS. Increasing evidence also indicates that long non-coding RNA H19 (lncRNA H19) involved in AS. However, whether the role of lncRNA H19 in AS is related to pyroptosis and the underlying mechanisms are largely unknown. In this study, we found that oxidized low-density lipoprotein (ox-LDL) induced pyroptosis and decreased the expression of lncRNA H19 in Raw 264.7 cells. Besides, silencing endogenous lncRNA H19 increased inflammatory responses and pyroptosis while exogenous overexpression of lncRNA H19 reversed this effect. Notably, we identified that the inhibitor of caspase-1 (XV-765) completely abrogated the silencing endogenous lncRNA H19 mediated pyroptosis. In addition, we found that lncRNA H19 inhibited ox-LDL-induced activation of nuclear factor-kappa B (NF-κB), mitochondrial dysfunction, and reduced the production of reactive oxygen species (ROS). Moreover, VX-765 impaired the silencing endogenous lncRNA H19 mediated pyroptosis. Overall, these findings indicated that lncRNA H19 may play an important role in pyroptosis and may serve as a potential therapeutic target for AS.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>34341910</pmid><doi>10.1007/s10753-021-01511-1</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0003-1503-3721</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0360-3997 |
| ispartof | Inflammation, 2021-12, Vol.44 (6), p.2407-2418 |
| issn | 0360-3997 1573-2576 |
| language | eng |
| recordid | cdi_proquest_journals_2602328372 |
| source | MEDLINE; SpringerNature Journals |
| subjects | Animals Apoptosis Arteriosclerosis Atherosclerosis Atherosclerosis - genetics Atherosclerosis - metabolism Atherosclerosis - pathology Biomedical and Life Sciences Biomedicine Blood vessels Caspase 1 - genetics Caspase 1 - metabolism Caspase-1 Cell activation Cell death Cell injury Chronic illnesses Cytokines Disease Immune system Immunology Inflammation Internal Medicine Lipids Lipoproteins Lipoproteins, LDL - toxicity Low density lipoprotein Macrophages - drug effects Macrophages - metabolism Macrophages - pathology Mice Mitochondria Mitochondria - drug effects Mitochondria - metabolism Mitochondria - pathology NF-kappa B - metabolism NF-κB protein Non-coding RNA Original Article Pathology Pharmacology/Toxicology Pyroptosis Pyroptosis - drug effects RAW 264.7 Cells Reactive oxygen species Reactive Oxygen Species - metabolism Rheumatology RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism Signal Transduction Smooth muscle |
| title | LncRNA H19 Mitigates Oxidized Low-Density Lipoprotein Induced Pyroptosis via Caspase-1 in Raw 264.7 Cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-02T00%3A49%3A44IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=LncRNA%20H19%20Mitigates%20Oxidized%20Low-Density%20Lipoprotein%20Induced%20Pyroptosis%20via%20Caspase-1%20in%20Raw%20264.7%20Cells&rft.jtitle=Inflammation&rft.au=Liu,%20Shan&rft.date=2021-12-01&rft.volume=44&rft.issue=6&rft.spage=2407&rft.epage=2418&rft.pages=2407-2418&rft.issn=0360-3997&rft.eissn=1573-2576&rft_id=info:doi/10.1007/s10753-021-01511-1&rft_dat=%3Cproquest_cross%3E2602328372%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2602328372&rft_id=info:pmid/34341910&rfr_iscdi=true |