Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG20099)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
mmu-miR-214-3p
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).
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Phospholipid hydroperoxide glutathione peroxidase (GPX4) [Suppressor]
| 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 | |||
| Pathway Response | Ferroptosis | hsa04216 | |||
| Fatty acid metabolism | hsa01212 | ||||
| Cell Process | Cell ferroptosis | ||||
In Vitro Model |
TCMK-1 cells | Normal | Mus musculus | CVCL_2772 | |
| In Vivo Model |
The C57BL/6 male mice (8-week-old, weighing approximately 20-25 g) were procured from Beijing Huafukang Bioscience Co. Inc. The mice were raised under the SPF condition. Cisplatin was injected into the mice intraperitoneally and only once at a dose of 30 mg/kg to induce AKI, while the control mice were injected with PBS. Intravenous administration of 10 mg/kg of agomir negative control (agomir NC) or agomir miR-214-3p (GenePharma Co. Ltd, Shanghai, China) was performed for the control group mice and model group mice, respectively. The ferroptosis inhibitor named Fer-1 (#S7243, Selleck Chemicals, Houston, TX, USA) was dissolved in DMSO and then diluted in 0.9% NaCl to prepare separate Fer-1 solutions each with a concentration of 0.2 mg/mL. Fer-1 was injected into the mice intraperitoneally, 1 h prior to injecting cisplatin, while the control mice received the injection of only 0.9% NaCl in 0.1% DMSO. Both experimental and control group mice were sacrificed at Day 1, 2, and 3, separately, post-cisplatin injection.
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| Response regulation | GPX4 was predicted as a target of miR-214-3p. Moreover, inhibiting miR-214-3p enhanced the expressions of GPX4 and SLC7A11 while decreasing the ACSL4 expression. Furthermore, miR-214-3p down-regulation protected against TEC death and renal tubule damage both in vitro and in vivo. According to these findings, inhibiting miR-214-3p would alleviate TEC ferroptosis in acute kidney injury (AKI) induced by cisplatin (cis-AKI) via GPX4. | ||||
Acute kidney failure [ICD-11: GB60]
| In total 1 item(s) under this disease | |||||
| Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
| Target Regulator | mmu-miR-214-3p (miRNA) | miRNA | |||
| Pathway Response | Ferroptosis | hsa04216 | |||
| Fatty acid metabolism | hsa01212 | ||||
| Cell Process | Cell ferroptosis | ||||
In Vitro Model |
TCMK-1 cells | Normal | Mus musculus | CVCL_2772 | |
| In Vivo Model |
The C57BL/6 male mice (8-week-old, weighing approximately 20-25 g) were procured from Beijing Huafukang Bioscience Co. Inc. The mice were raised under the SPF condition. Cisplatin was injected into the mice intraperitoneally and only once at a dose of 30 mg/kg to induce AKI, while the control mice were injected with PBS. Intravenous administration of 10 mg/kg of agomir negative control (agomir NC) or agomir miR-214-3p (GenePharma Co. Ltd, Shanghai, China) was performed for the control group mice and model group mice, respectively. The ferroptosis inhibitor named Fer-1 (#S7243, Selleck Chemicals, Houston, TX, USA) was dissolved in DMSO and then diluted in 0.9% NaCl to prepare separate Fer-1 solutions each with a concentration of 0.2 mg/mL. Fer-1 was injected into the mice intraperitoneally, 1 h prior to injecting cisplatin, while the control mice received the injection of only 0.9% NaCl in 0.1% DMSO. Both experimental and control group mice were sacrificed at Day 1, 2, and 3, separately, post-cisplatin injection.
Click to Show/Hide
|
||||
| Response regulation | GPX4 was predicted as a target of miR-214-3p. Moreover, inhibiting miR-214-3p enhanced the expressions of GPX4 and SLC7A11 while decreasing the ACSL4 expression. Furthermore, miR-214-3p down-regulation protected against TEC death and renal tubule damage both in vitro and in vivo. According to these findings, inhibiting miR-214-3p would alleviate TEC ferroptosis in acute kidney injury (AKI) induced by cisplatin (cis-AKI) via GPX4. | ||||