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...
Gespeichert in:
Veröffentlicht in: | The Journal of steroid biochemistry and molecular biology 2021-02, Vol.206, p.105789-105789, Article 105789 |
---|---|
Hauptverfasser: | , , , , , , , , , |
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 & 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 |