Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG20097)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
mmu-miR-15a-5p
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 myocardial infarction | ICD-11: BA41 | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Ferroptosis | hsa04216 | ||||
| Cell Process | Cell ferroptosis | ||||
| Cell proliferation | |||||
In Vitro Model |
HL-1 cells | Normal | Mus musculus | CVCL_0303 | |
| In Vivo Model |
The male C57BL/6 mice (20-25 g, 10-week-old) were purchased from the Experimental Animal Center of Harbin Medical University (Harbin, China). Mice were anaesthetized with pentobarbital sodium (30 mg/kg, Sigma-Aldrich, St. Louis, USA) by intraperitoneal injection. The animals were fixed on the operating table in supine position, and the chest were sterilized and opened by blunt separation at the left 4th intercosal space. In the model group, the left anterior descending artery (LAD) was ligated with 7/0 silk suture for 3 days.
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| Response regulation | GPX4 was the direct target of miR-15a-5p by luciferase reporter assay. Mechanistically, silencing transcription factor early growth response-1 (Egr-1) inhibited the level of miR-15a-5p, increased the protein expression of GPX4, accompanied by reduced ferroptosis and alleviated myocardial injury. These results provide a novel signaling pathway during the progression of acute myocardial infarction, namely Egr-1/miR-15a-5p/GPX4/ferroptosis. | ||||
Acute myocardial infarction [ICD-11: BA41]
| In total 1 item(s) under this disease | |||||
| Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
| Target Regulator | mmu-miR-15a-5p (miRNA) | miRNA | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Ferroptosis | hsa04216 | ||||
| Cell Process | Cell ferroptosis | ||||
| Cell proliferation | |||||
In Vitro Model |
HL-1 cells | Normal | Mus musculus | CVCL_0303 | |
| In Vivo Model |
The male C57BL/6 mice (20-25 g, 10-week-old) were purchased from the Experimental Animal Center of Harbin Medical University (Harbin, China). Mice were anaesthetized with pentobarbital sodium (30 mg/kg, Sigma-Aldrich, St. Louis, USA) by intraperitoneal injection. The animals were fixed on the operating table in supine position, and the chest were sterilized and opened by blunt separation at the left 4th intercosal space. In the model group, the left anterior descending artery (LAD) was ligated with 7/0 silk suture for 3 days.
Click to Show/Hide
|
||||
| Response regulation | GPX4 was the direct target of miR-15a-5p by luciferase reporter assay. Mechanistically, silencing transcription factor early growth response-1 (Egr-1) inhibited the level of miR-15a-5p, increased the protein expression of GPX4, accompanied by reduced ferroptosis and alleviated myocardial injury. These results provide a novel signaling pathway during the progression of acute myocardial infarction, namely Egr-1/miR-15a-5p/GPX4/ferroptosis. | ||||