Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG10110)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
EGR1
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. | ||||
Unspecific Target [Unspecific Target]
| In total 1 item(s) under this target | |||||
| Experiment 1 Reporting the Ferroptosis Target of This Regulator | [2] | ||||
| Responsed Disease | Intervertebral disc degeneration | ICD-11: FA80 | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Ferroptosis | hsa04216 | ||||
| NF-kappa B signaling pathway | hsa04064 | ||||
| Cell Process | Cell ferroptosis | ||||
In Vitro Model |
hCEPs (Human cartilage endplate cells) | ||||
| In Vivo Model |
24 male C57BL/6J mice (8 weeks, weighing 20 ± 2 g) were purchased from Charles River (Beijing, China). Mice were anesthetized via an intraperitoneal injection of 3% pentobarbital sodium (40 mg/kg). Afterward, their extraperitoneal space was isolated and the exterior part of IVD was exposed. A 26 G puncture needle (90% of intervertebral space height) was utilized to punch in the C6/C7 IVD at a depth of 2.5 mm. The puncture needle was inserted into the dorsal annulus fibrosus across the center of the nucleus pulposus and partially across the ventral annulus fibrosus and withdrawn 30 s later.
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| Response regulation | In Intervertebral disc degeneration (IVDD) cell models, EGR1 knockdown reduced ferroptosis and cartilage degeneration, which was reversed by MAP3K14 overexpression or Erastin treatment. Collectively, EGR1 promoted ferroptosis and IVD cartilage degeneration through MAP3K14-NF-B axis. | ||||
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 | Early growth response protein 1 (EGR1) | Protein coding | |||
| 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. | ||||
Intervertebral disc degeneration [ICD-11: FA80]
| In total 1 item(s) under this disease | |||||
| Experiment 1 Reporting the Ferroptosis-centered Disease Response | [2] | ||||
| Target Regulator | Early growth response protein 1 (EGR1) | Protein coding | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Ferroptosis | hsa04216 | ||||
| NF-kappa B signaling pathway | hsa04064 | ||||
| Cell Process | Cell ferroptosis | ||||
In Vitro Model |
hCEPs (Human cartilage endplate cells) | ||||
| In Vivo Model |
24 male C57BL/6J mice (8 weeks, weighing 20 ± 2 g) were purchased from Charles River (Beijing, China). Mice were anesthetized via an intraperitoneal injection of 3% pentobarbital sodium (40 mg/kg). Afterward, their extraperitoneal space was isolated and the exterior part of IVD was exposed. A 26 G puncture needle (90% of intervertebral space height) was utilized to punch in the C6/C7 IVD at a depth of 2.5 mm. The puncture needle was inserted into the dorsal annulus fibrosus across the center of the nucleus pulposus and partially across the ventral annulus fibrosus and withdrawn 30 s later.
Click to Show/Hide
|
||||
| Response regulation | In Intervertebral disc degeneration (IVDD) cell models, EGR1 knockdown reduced ferroptosis and cartilage degeneration, which was reversed by MAP3K14 overexpression or Erastin treatment. Collectively, EGR1 promoted ferroptosis and IVD cartilage degeneration through MAP3K14-NF-B axis. | ||||
References