Vitamin D/VDR attenuate cisplatin-induced AKI by down-regulating NLRP3/Caspase-1/GSDMD pyroptosis pathway

•The experiment found thatvitamin D / VDR can inhibiting cell pyrolysis in cisplatin-induced AKI.•The experiment used tubule-specific overexpression mice in cisplatin-induced AKI.•The experiment separately observed the role of VDR in cisplatin-induced AKI. Vitamin D/Vitamin D receptor (VDR) has been...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:The Journal of steroid biochemistry and molecular biology 2021-02, Vol.206, p.105789-105789, Article 105789
Hauptverfasser: Jiang, Siqing, Zhang, Hao, Li, Xin, Yi, Bin, Huang, Lihua, Hu, Zhaoxin, Li, Aimei, Du, Jie, Li, Yanchun, Zhang, Wei
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 105789
container_issue
container_start_page 105789
container_title The Journal of steroid biochemistry and molecular biology
container_volume 206
creator Jiang, Siqing
Zhang, Hao
Li, Xin
Yi, Bin
Huang, Lihua
Hu, Zhaoxin
Li, Aimei
Du, Jie
Li, Yanchun
Zhang, Wei
description •The experiment found thatvitamin D / VDR can inhibiting cell pyrolysis in cisplatin-induced AKI.•The experiment used tubule-specific overexpression mice in cisplatin-induced AKI.•The experiment separately observed the role of VDR in cisplatin-induced AKI. Vitamin D/Vitamin D receptor (VDR) has been shown to inhibit the NF-κB-mediated inflammatory effects. Up-regulation of the NLRP3(Recombinant NLR Family, Pyrin Domain Containing Protein 3)/Caspase-1/GSDMD (Gasdermin D) pathway through NF-κb is one of the key mechanisms leading to pyroptosis. This study aims to explore the effects of vitamin D/VDR on the pyroptosis pathway in cisplatin induced acute kidney injury (AKI) models. Our results showed that in wide type mice, renal function loss, tissue injury and cell death induced by cisplatin were alleviated by pretreatment of high-dose paricalcitol(a VDR agonist) accompanied with up-regulated VDR and decreased expression of NLRP3, GSDMD-N, Cleaved-Caspase-1 and mature Interleukin- 1β (features of pyroptosis). While, in VDR knock out mice, cisplatin induced more severer renal injury and further increased pyroptosis related protein than the wild type mice and the effect of paricalcitol were also eliminated. In tubular cell specific VDR-over expressing mice, those renal injury index as well as pyroptosis phenotype were significantly reduced by low-dose paricalcitol pretreatment with upregulated VDR expression compared with WT mice. In vitro data using gain and lose function experiments in Human tubular epithelial cell (HK-2) were consistent with the observation as in vivo work. Our further experiments in both animal and cell culture work has found that the level of IκBα(Inhibitor of NF-κB) were decreased and the nuclear level of NF-κB p65 of renal tubular cells were increased after cisplatin injury while VDR activation by paricalcitol could reverse up-regulation of nuclear NF-κB p65 with reduced cell pyroptosis. These data suggested that vitamin D/VDR could alleviate cisplatin-induced acute renal injury partly by inhibiting NF-κB-mediated NLRP3/Caspase-1/GSDMD pyroptosis.
doi_str_mv 10.1016/j.jsbmb.2020.105789
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2466292733</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0960076020303149</els_id><sourcerecordid>2488247045</sourcerecordid><originalsourceid>FETCH-LOGICAL-c387t-a15534be8534ed427ba7eba54b822867f49b5060fb17f7835db4c8549f47d953</originalsourceid><addsrcrecordid>eNp9kUtvEzEUhS0EomnhFyAhS2zYTOLn2F6wqBIoFeGhUnVr2TN3ikeZR20PVf59J01hwYKNLdnfOffqHITeULKkhJardtkm3_klI-zwIpU2z9CCamUKyhh5jhbElKQgqiQn6DSllhDCOVUv0QnnTBrD9QKFm5BdF3q8Wd1srrDLGfrJZcBVSOPO5dAXoa-nCmp8_uUS-z2uh_u-iHA7Pf7e4m_bqx98tXZpdAkKurr4ufm6weM-DmMeUkh4dPnXvdu_Qi8at0vw-uk-Q9efPl6vPxfb7xeX6_NtUXGtcuGolFx40PMJtWDKOwXeSeE1Y7pUjTBekpI0nqpGaS5rLyothWmEqo3kZ-j90XaMw90EKdsupAp2O9fDMCXLRFkywxTnM_ruH7QdptjPy82U1kwoIg6G_EhVcUgpQmPHGDoX95YSeyjCtvaxCHsowh6LmFVvn7wn30H9V_Mn-Rn4cARgzuJ3gGhTFaCfgw4RqmzrIfx3wAORaJhc</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2488247045</pqid></control><display><type>article</type><title>Vitamin D/VDR attenuate cisplatin-induced AKI by down-regulating NLRP3/Caspase-1/GSDMD pyroptosis pathway</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><creator>Jiang, Siqing ; Zhang, Hao ; Li, Xin ; Yi, Bin ; Huang, Lihua ; Hu, Zhaoxin ; Li, Aimei ; Du, Jie ; Li, Yanchun ; Zhang, Wei</creator><creatorcontrib>Jiang, Siqing ; Zhang, Hao ; Li, Xin ; Yi, Bin ; Huang, Lihua ; Hu, Zhaoxin ; Li, Aimei ; Du, Jie ; Li, Yanchun ; Zhang, Wei</creatorcontrib><description>•The experiment found thatvitamin D / VDR can inhibiting cell pyrolysis in cisplatin-induced AKI.•The experiment used tubule-specific overexpression mice in cisplatin-induced AKI.•The experiment separately observed the role of VDR in cisplatin-induced AKI. Vitamin D/Vitamin D receptor (VDR) has been shown to inhibit the NF-κB-mediated inflammatory effects. Up-regulation of the NLRP3(Recombinant NLR Family, Pyrin Domain Containing Protein 3)/Caspase-1/GSDMD (Gasdermin D) pathway through NF-κb is one of the key mechanisms leading to pyroptosis. This study aims to explore the effects of vitamin D/VDR on the pyroptosis pathway in cisplatin induced acute kidney injury (AKI) models. Our results showed that in wide type mice, renal function loss, tissue injury and cell death induced by cisplatin were alleviated by pretreatment of high-dose paricalcitol(a VDR agonist) accompanied with up-regulated VDR and decreased expression of NLRP3, GSDMD-N, Cleaved-Caspase-1 and mature Interleukin- 1β (features of pyroptosis). While, in VDR knock out mice, cisplatin induced more severer renal injury and further increased pyroptosis related protein than the wild type mice and the effect of paricalcitol were also eliminated. In tubular cell specific VDR-over expressing mice, those renal injury index as well as pyroptosis phenotype were significantly reduced by low-dose paricalcitol pretreatment with upregulated VDR expression compared with WT mice. In vitro data using gain and lose function experiments in Human tubular epithelial cell (HK-2) were consistent with the observation as in vivo work. Our further experiments in both animal and cell culture work has found that the level of IκBα(Inhibitor of NF-κB) were decreased and the nuclear level of NF-κB p65 of renal tubular cells were increased after cisplatin injury while VDR activation by paricalcitol could reverse up-regulation of nuclear NF-κB p65 with reduced cell pyroptosis. These data suggested that vitamin D/VDR could alleviate cisplatin-induced acute renal injury partly by inhibiting NF-κB-mediated NLRP3/Caspase-1/GSDMD pyroptosis.</description><identifier>ISSN: 0960-0760</identifier><identifier>EISSN: 1879-1220</identifier><identifier>DOI: 10.1016/j.jsbmb.2020.105789</identifier><identifier>PMID: 33259938</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Acute kidney injury ; Acute Kidney Injury - chemically induced ; Acute Kidney Injury - drug therapy ; Acute Kidney Injury - genetics ; Acute Kidney Injury - pathology ; Animals ; Caspase 1 - genetics ; Caspase-1 ; Cell culture ; Cell death ; Cisplatin ; Cisplatin - adverse effects ; Epithelial cells ; Ergocalciferols - pharmacology ; Gene Expression Regulation - drug effects ; Humans ; Inflammation ; Intracellular Signaling Peptides and Proteins - genetics ; Kidney - drug effects ; Kidney - injuries ; Kidney - pathology ; Mice ; Mice, Knockout ; NF-κB pathway ; NF-κB protein ; NLR Family, Pyrin Domain-Containing 3 Protein - genetics ; Phenotypes ; Phosphate-Binding Proteins - genetics ; Pyrin protein ; Pyroptosis ; Pyroptosis - drug effects ; Pyroptosis - genetics ; Pyroptosis pathway ; Receptors, Calcitriol - genetics ; Renal function ; Vitamin D ; Vitamin D - pharmacology ; Vitamin D receptor ; Vitamin D receptors</subject><ispartof>The Journal of steroid biochemistry and molecular biology, 2021-02, Vol.206, p.105789-105789, Article 105789</ispartof><rights>2020 Elsevier Ltd</rights><rights>Copyright © 2020 Elsevier Ltd. All rights reserved.</rights><rights>Copyright Elsevier BV Feb 2021</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c387t-a15534be8534ed427ba7eba54b822867f49b5060fb17f7835db4c8549f47d953</citedby><cites>FETCH-LOGICAL-c387t-a15534be8534ed427ba7eba54b822867f49b5060fb17f7835db4c8549f47d953</cites><orcidid>0000-0002-0699-9201</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0960076020303149$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33259938$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jiang, Siqing</creatorcontrib><creatorcontrib>Zhang, Hao</creatorcontrib><creatorcontrib>Li, Xin</creatorcontrib><creatorcontrib>Yi, Bin</creatorcontrib><creatorcontrib>Huang, Lihua</creatorcontrib><creatorcontrib>Hu, Zhaoxin</creatorcontrib><creatorcontrib>Li, Aimei</creatorcontrib><creatorcontrib>Du, Jie</creatorcontrib><creatorcontrib>Li, Yanchun</creatorcontrib><creatorcontrib>Zhang, Wei</creatorcontrib><title>Vitamin D/VDR attenuate cisplatin-induced AKI by down-regulating NLRP3/Caspase-1/GSDMD pyroptosis pathway</title><title>The Journal of steroid biochemistry and molecular biology</title><addtitle>J Steroid Biochem Mol Biol</addtitle><description>•The experiment found thatvitamin D / VDR can inhibiting cell pyrolysis in cisplatin-induced AKI.•The experiment used tubule-specific overexpression mice in cisplatin-induced AKI.•The experiment separately observed the role of VDR in cisplatin-induced AKI. Vitamin D/Vitamin D receptor (VDR) has been shown to inhibit the NF-κB-mediated inflammatory effects. Up-regulation of the NLRP3(Recombinant NLR Family, Pyrin Domain Containing Protein 3)/Caspase-1/GSDMD (Gasdermin D) pathway through NF-κb is one of the key mechanisms leading to pyroptosis. This study aims to explore the effects of vitamin D/VDR on the pyroptosis pathway in cisplatin induced acute kidney injury (AKI) models. Our results showed that in wide type mice, renal function loss, tissue injury and cell death induced by cisplatin were alleviated by pretreatment of high-dose paricalcitol(a VDR agonist) accompanied with up-regulated VDR and decreased expression of NLRP3, GSDMD-N, Cleaved-Caspase-1 and mature Interleukin- 1β (features of pyroptosis). While, in VDR knock out mice, cisplatin induced more severer renal injury and further increased pyroptosis related protein than the wild type mice and the effect of paricalcitol were also eliminated. In tubular cell specific VDR-over expressing mice, those renal injury index as well as pyroptosis phenotype were significantly reduced by low-dose paricalcitol pretreatment with upregulated VDR expression compared with WT mice. In vitro data using gain and lose function experiments in Human tubular epithelial cell (HK-2) were consistent with the observation as in vivo work. Our further experiments in both animal and cell culture work has found that the level of IκBα(Inhibitor of NF-κB) were decreased and the nuclear level of NF-κB p65 of renal tubular cells were increased after cisplatin injury while VDR activation by paricalcitol could reverse up-regulation of nuclear NF-κB p65 with reduced cell pyroptosis. These data suggested that vitamin D/VDR could alleviate cisplatin-induced acute renal injury partly by inhibiting NF-κB-mediated NLRP3/Caspase-1/GSDMD pyroptosis.</description><subject>Acute kidney injury</subject><subject>Acute Kidney Injury - chemically induced</subject><subject>Acute Kidney Injury - drug therapy</subject><subject>Acute Kidney Injury - genetics</subject><subject>Acute Kidney Injury - pathology</subject><subject>Animals</subject><subject>Caspase 1 - genetics</subject><subject>Caspase-1</subject><subject>Cell culture</subject><subject>Cell death</subject><subject>Cisplatin</subject><subject>Cisplatin - adverse effects</subject><subject>Epithelial cells</subject><subject>Ergocalciferols - pharmacology</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Intracellular Signaling Peptides and Proteins - genetics</subject><subject>Kidney - drug effects</subject><subject>Kidney - injuries</subject><subject>Kidney - pathology</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>NF-κB pathway</subject><subject>NF-κB protein</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein - genetics</subject><subject>Phenotypes</subject><subject>Phosphate-Binding Proteins - genetics</subject><subject>Pyrin protein</subject><subject>Pyroptosis</subject><subject>Pyroptosis - drug effects</subject><subject>Pyroptosis - genetics</subject><subject>Pyroptosis pathway</subject><subject>Receptors, Calcitriol - genetics</subject><subject>Renal function</subject><subject>Vitamin D</subject><subject>Vitamin D - pharmacology</subject><subject>Vitamin D receptor</subject><subject>Vitamin D receptors</subject><issn>0960-0760</issn><issn>1879-1220</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kUtvEzEUhS0EomnhFyAhS2zYTOLn2F6wqBIoFeGhUnVr2TN3ikeZR20PVf59J01hwYKNLdnfOffqHITeULKkhJardtkm3_klI-zwIpU2z9CCamUKyhh5jhbElKQgqiQn6DSllhDCOVUv0QnnTBrD9QKFm5BdF3q8Wd1srrDLGfrJZcBVSOPO5dAXoa-nCmp8_uUS-z2uh_u-iHA7Pf7e4m_bqx98tXZpdAkKurr4ufm6weM-DmMeUkh4dPnXvdu_Qi8at0vw-uk-Q9efPl6vPxfb7xeX6_NtUXGtcuGolFx40PMJtWDKOwXeSeE1Y7pUjTBekpI0nqpGaS5rLyothWmEqo3kZ-j90XaMw90EKdsupAp2O9fDMCXLRFkywxTnM_ruH7QdptjPy82U1kwoIg6G_EhVcUgpQmPHGDoX95YSeyjCtvaxCHsowh6LmFVvn7wn30H9V_Mn-Rn4cARgzuJ3gGhTFaCfgw4RqmzrIfx3wAORaJhc</recordid><startdate>202102</startdate><enddate>202102</enddate><creator>Jiang, Siqing</creator><creator>Zhang, Hao</creator><creator>Li, Xin</creator><creator>Yi, Bin</creator><creator>Huang, Lihua</creator><creator>Hu, Zhaoxin</creator><creator>Li, Aimei</creator><creator>Du, Jie</creator><creator>Li, Yanchun</creator><creator>Zhang, Wei</creator><general>Elsevier Ltd</general><general>Elsevier BV</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>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-0699-9201</orcidid></search><sort><creationdate>202102</creationdate><title>Vitamin D/VDR attenuate cisplatin-induced AKI by down-regulating NLRP3/Caspase-1/GSDMD pyroptosis pathway</title><author>Jiang, Siqing ; Zhang, Hao ; Li, Xin ; Yi, Bin ; Huang, Lihua ; Hu, Zhaoxin ; Li, Aimei ; Du, Jie ; Li, Yanchun ; Zhang, Wei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c387t-a15534be8534ed427ba7eba54b822867f49b5060fb17f7835db4c8549f47d953</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Acute kidney injury</topic><topic>Acute Kidney Injury - chemically induced</topic><topic>Acute Kidney Injury - drug therapy</topic><topic>Acute Kidney Injury - genetics</topic><topic>Acute Kidney Injury - pathology</topic><topic>Animals</topic><topic>Caspase 1 - genetics</topic><topic>Caspase-1</topic><topic>Cell culture</topic><topic>Cell death</topic><topic>Cisplatin</topic><topic>Cisplatin - adverse effects</topic><topic>Epithelial cells</topic><topic>Ergocalciferols - pharmacology</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Intracellular Signaling Peptides and Proteins - genetics</topic><topic>Kidney - drug effects</topic><topic>Kidney - injuries</topic><topic>Kidney - pathology</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>NF-κB pathway</topic><topic>NF-κB protein</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein - genetics</topic><topic>Phenotypes</topic><topic>Phosphate-Binding Proteins - genetics</topic><topic>Pyrin protein</topic><topic>Pyroptosis</topic><topic>Pyroptosis - drug effects</topic><topic>Pyroptosis - genetics</topic><topic>Pyroptosis pathway</topic><topic>Receptors, Calcitriol - genetics</topic><topic>Renal function</topic><topic>Vitamin D</topic><topic>Vitamin D - pharmacology</topic><topic>Vitamin D receptor</topic><topic>Vitamin D receptors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jiang, Siqing</creatorcontrib><creatorcontrib>Zhang, Hao</creatorcontrib><creatorcontrib>Li, Xin</creatorcontrib><creatorcontrib>Yi, Bin</creatorcontrib><creatorcontrib>Huang, Lihua</creatorcontrib><creatorcontrib>Hu, Zhaoxin</creatorcontrib><creatorcontrib>Li, Aimei</creatorcontrib><creatorcontrib>Du, Jie</creatorcontrib><creatorcontrib>Li, Yanchun</creatorcontrib><creatorcontrib>Zhang, Wei</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of steroid biochemistry and molecular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jiang, Siqing</au><au>Zhang, Hao</au><au>Li, Xin</au><au>Yi, Bin</au><au>Huang, Lihua</au><au>Hu, Zhaoxin</au><au>Li, Aimei</au><au>Du, Jie</au><au>Li, Yanchun</au><au>Zhang, Wei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Vitamin D/VDR attenuate cisplatin-induced AKI by down-regulating NLRP3/Caspase-1/GSDMD pyroptosis pathway</atitle><jtitle>The Journal of steroid biochemistry and molecular biology</jtitle><addtitle>J Steroid Biochem Mol Biol</addtitle><date>2021-02</date><risdate>2021</risdate><volume>206</volume><spage>105789</spage><epage>105789</epage><pages>105789-105789</pages><artnum>105789</artnum><issn>0960-0760</issn><eissn>1879-1220</eissn><abstract>•The experiment found thatvitamin D / VDR can inhibiting cell pyrolysis in cisplatin-induced AKI.•The experiment used tubule-specific overexpression mice in cisplatin-induced AKI.•The experiment separately observed the role of VDR in cisplatin-induced AKI. Vitamin D/Vitamin D receptor (VDR) has been shown to inhibit the NF-κB-mediated inflammatory effects. Up-regulation of the NLRP3(Recombinant NLR Family, Pyrin Domain Containing Protein 3)/Caspase-1/GSDMD (Gasdermin D) pathway through NF-κb is one of the key mechanisms leading to pyroptosis. This study aims to explore the effects of vitamin D/VDR on the pyroptosis pathway in cisplatin induced acute kidney injury (AKI) models. Our results showed that in wide type mice, renal function loss, tissue injury and cell death induced by cisplatin were alleviated by pretreatment of high-dose paricalcitol(a VDR agonist) accompanied with up-regulated VDR and decreased expression of NLRP3, GSDMD-N, Cleaved-Caspase-1 and mature Interleukin- 1β (features of pyroptosis). While, in VDR knock out mice, cisplatin induced more severer renal injury and further increased pyroptosis related protein than the wild type mice and the effect of paricalcitol were also eliminated. In tubular cell specific VDR-over expressing mice, those renal injury index as well as pyroptosis phenotype were significantly reduced by low-dose paricalcitol pretreatment with upregulated VDR expression compared with WT mice. In vitro data using gain and lose function experiments in Human tubular epithelial cell (HK-2) were consistent with the observation as in vivo work. Our further experiments in both animal and cell culture work has found that the level of IκBα(Inhibitor of NF-κB) were decreased and the nuclear level of NF-κB p65 of renal tubular cells were increased after cisplatin injury while VDR activation by paricalcitol could reverse up-regulation of nuclear NF-κB p65 with reduced cell pyroptosis. These data suggested that vitamin D/VDR could alleviate cisplatin-induced acute renal injury partly by inhibiting NF-κB-mediated NLRP3/Caspase-1/GSDMD pyroptosis.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>33259938</pmid><doi>10.1016/j.jsbmb.2020.105789</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-0699-9201</orcidid></addata></record>
fulltext fulltext
identifier ISSN: 0960-0760
ispartof The Journal of steroid biochemistry and molecular biology, 2021-02, Vol.206, p.105789-105789, Article 105789
issn 0960-0760
1879-1220
language eng
recordid cdi_proquest_miscellaneous_2466292733
source MEDLINE; Elsevier ScienceDirect Journals
subjects Acute kidney injury
Acute Kidney Injury - chemically induced
Acute Kidney Injury - drug therapy
Acute Kidney Injury - genetics
Acute Kidney Injury - pathology
Animals
Caspase 1 - genetics
Caspase-1
Cell culture
Cell death
Cisplatin
Cisplatin - adverse effects
Epithelial cells
Ergocalciferols - pharmacology
Gene Expression Regulation - drug effects
Humans
Inflammation
Intracellular Signaling Peptides and Proteins - genetics
Kidney - drug effects
Kidney - injuries
Kidney - pathology
Mice
Mice, Knockout
NF-κB pathway
NF-κB protein
NLR Family, Pyrin Domain-Containing 3 Protein - genetics
Phenotypes
Phosphate-Binding Proteins - genetics
Pyrin protein
Pyroptosis
Pyroptosis - drug effects
Pyroptosis - genetics
Pyroptosis pathway
Receptors, Calcitriol - genetics
Renal function
Vitamin D
Vitamin D - pharmacology
Vitamin D receptor
Vitamin D receptors
title Vitamin D/VDR attenuate cisplatin-induced AKI by down-regulating NLRP3/Caspase-1/GSDMD pyroptosis pathway
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-30T05%3A40%3A55IST&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=Vitamin%20D/VDR%20attenuate%20cisplatin-induced%20AKI%20by%20down-regulating%20NLRP3/Caspase-1/GSDMD%20pyroptosis%20pathway&rft.jtitle=The%20Journal%20of%20steroid%20biochemistry%20and%20molecular%20biology&rft.au=Jiang,%20Siqing&rft.date=2021-02&rft.volume=206&rft.spage=105789&rft.epage=105789&rft.pages=105789-105789&rft.artnum=105789&rft.issn=0960-0760&rft.eissn=1879-1220&rft_id=info:doi/10.1016/j.jsbmb.2020.105789&rft_dat=%3Cproquest_cross%3E2488247045%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=2488247045&rft_id=info:pmid/33259938&rft_els_id=S0960076020303149&rfr_iscdi=true