Ferroptosis Regulator Information

General Information of the Ferroptosis Regulator (ID: REG10092)
Regulator Name Vitamin D3 receptor (VDR)
Synonyms
NR1I1; 1,25-dihydroxyvitamin D3 receptor; Nuclear receptor subfamily 1 group I member 1
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Gene Name VDR
Gene ID 7421
Regulator Type Protein coding
Uniprot ID P11473
Sequence
MEAMAASTSLPDPGDFDRNVPRICGVCGDRATGFHFNAMTCEGCKGFFRRSMKRKALFTC
PFNGDCRITKDNRRHCQACRLKRCVDIGMMKEFILTDEEVQRKREMILKRKEEEALKDSL
RPKLSEEQQRIIAILLDAHHKTYDPTYSDFCQFRPPVRVNDGGGSHPSRPNSRHTPSFSG
DSSSSCSDHCITSSDMMDSSSFSNLDLSEEDSDDPSVTLELSQLSMLPHLADLVSYSIQK
VIGFAKMIPGFRDLTSEDQIVLLKSSAIEVIMLRSNESFTMDDMSWTCGNQDYKYRVSDV
TKAGHSLELIEPLIKFQVGLKKLNLHEEEHVLLMAICIVSPDRPGVQDAALIEAIQDRLS
NTLQTYIRCRHPPPGSHLLYAKMIQKLADLRSLNEEHSKQYRCLSFQPECSMKLTPLVLE
VFGNEIS

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Family Nuclear hormone receptor family
Function
Nuclear receptor for calcitriol, the active form of vitamin D3 which mediates the action of this vitamin on cells. Enters the nucleus upon vitamin D3 binding where it forms heterodimers with the retinoid X receptor/RXR. The VDR-RXR heterodimers bind to specific response elements on DNA and activate the transcription of vitamin D3-responsive target genes. Plays a central role in calcium homeostasis. Also functions as a receptor for the secondary bile acid lithocholic acid (LCA) and its metabolites.

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HGNC ID
HGNC:12679
KEGG ID hsa:7421
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
VDR can regulate the following target(s), and cause disease/drug response(s). You can browse detail information of target(s) or disease/drug response(s).
Browse Target
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Phospholipid hydroperoxide glutathione peroxidase (GPX4) [Suppressor]
 Target Info 
In total 1 item(s) under this target
Experiment 1 Reporting the Ferroptosis Target of This Regulator [1]
Target for Ferroptosis Suppressor
Responsed Disease Acute kidney failure ICD-11: GB60
 Disease Info 
Responsed Drug Paricalcitol Approved
 Drug Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model
 HK-2 cells Normal Homo sapiens CVCL_0302
In Vivo Model
A total of 72 male C57BL/6 mice were purchased from Slyke jingda Biotechnology Company. They were randomly divided into five groups: Control group (n = 8), Cisplatin (20 mg/kg dissolved in saline) only group (n = 16), Cisplatin + paricalcitol (0.2 ug/kg dissolved in sterile water for injection and 20% propylene glycol) group (n = 16), Cisplatin + DMSO group (n = 16), Cisplatin + Fer-1 (5 mg/kg dissolved in DMSO) group (n = 16), were administered intraperitoneally. Cisplatin was injected once to mice, while Fer-1 was injected once an hour before cisplatin, and paricalcitol was injected once daily for five consecutive days before cisplatin. Each eight mice were sacrificed at 48 h and 72 h, respectively after cisplatin injection, and eight mice in the control group were sacrificed together with mice at 72 h.

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Response regulation Pretreatment of paricalcitol could also alleviated Erastin (an inducer of ferroptosis) induced cell death in HK-2 cell. Ferroptosis plays an important role in cisplatin induced acute kidney injury. VDR activation can protect against cisplatin induced renal injury by inhibiting ferroptosis partly via trans-regulation of GPX4.
Acute kidney failure [ICD-11: GB60]
 Disease Info 
In total 1 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response [1]
Target Regulator Vitamin D3 receptor (VDR) Protein coding
 Regulator Info 
Responsed Drug Paricalcitol Approved
 Drug Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model
 HK-2 cells Normal Homo sapiens CVCL_0302
In Vivo Model
A total of 72 male C57BL/6 mice were purchased from Slyke jingda Biotechnology Company. They were randomly divided into five groups: Control group (n = 8), Cisplatin (20 mg/kg dissolved in saline) only group (n = 16), Cisplatin + paricalcitol (0.2 ug/kg dissolved in sterile water for injection and 20% propylene glycol) group (n = 16), Cisplatin + DMSO group (n = 16), Cisplatin + Fer-1 (5 mg/kg dissolved in DMSO) group (n = 16), were administered intraperitoneally. Cisplatin was injected once to mice, while Fer-1 was injected once an hour before cisplatin, and paricalcitol was injected once daily for five consecutive days before cisplatin. Each eight mice were sacrificed at 48 h and 72 h, respectively after cisplatin injection, and eight mice in the control group were sacrificed together with mice at 72 h.

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Response regulation Pretreatment of paricalcitol could also alleviated Erastin (an inducer of ferroptosis) induced cell death in HK-2 cell. Ferroptosis plays an important role in cisplatin induced acute kidney injury. VDR activation can protect against cisplatin induced renal injury by inhibiting ferroptosis partly via trans-regulation of GPX4.
Paricalcitol [Approved]
 Drug Info 
In total 1 item(s) under this drug
Experiment 1 Reporting the Ferroptosis-centered Drug Response [1]
Drug for Ferroptosis Suppressor
Response Target Phospholipid hydroperoxide glutathione peroxidase (GPX4) Suppressor
 Target Info 
Responsed Disease Acute kidney failure ICD-11: GB60
 Disease Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model
 HK-2 cells Normal Homo sapiens CVCL_0302
In Vivo Model
A total of 72 male C57BL/6 mice were purchased from Slyke jingda Biotechnology Company. They were randomly divided into five groups: Control group (n = 8), Cisplatin (20 mg/kg dissolved in saline) only group (n = 16), Cisplatin + paricalcitol (0.2 ug/kg dissolved in sterile water for injection and 20% propylene glycol) group (n = 16), Cisplatin + DMSO group (n = 16), Cisplatin + Fer-1 (5 mg/kg dissolved in DMSO) group (n = 16), were administered intraperitoneally. Cisplatin was injected once to mice, while Fer-1 was injected once an hour before cisplatin, and paricalcitol was injected once daily for five consecutive days before cisplatin. Each eight mice were sacrificed at 48 h and 72 h, respectively after cisplatin injection, and eight mice in the control group were sacrificed together with mice at 72 h.

    Click to Show/Hide
Response regulation Pretreatment of paricalcitol could also alleviated Erastin (an inducer of ferroptosis) induced cell death in HK-2 cell. Ferroptosis plays an important role in cisplatin induced acute kidney injury. VDR activation can protect against cisplatin induced renal injury by inhibiting ferroptosis partly via trans-regulation of GPX4.
References
Ref 1 VDR activation attenuate cisplatin induced AKI by inhibiting ferroptosis. Cell Death Dis. 2020 Jan 29;11(1):73. doi: 10.1038/s41419-020-2256-z.