Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG10193)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
DHODH
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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Polyunsaturated fatty acid lipoxygenase ALOX15 (ALOX15) [Driver]
In total 2 item(s) under this target | |||||
Experiment 1 Reporting the Ferroptosis Target of This Regulator | [1] | ||||
Target for Ferroptosis | Driver | ||||
Responsed Disease | Spinal cord injury | ICD-11: ND51 | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
PC12 cells | Adrenal gland pheochromocytoma | Rattus norvegicus | CVCL_0481 | |
In Vivo Model |
Forty female Sprague-Dawley rats (200-300 g, 8 weeks old) were purchased from the Animal Experiment Center of Fudan University. Forty rats were randomly divided into four groups: sham operation group (n = 10), SCI group (n = 10), SCI + ferroptosis inhibitor group (SCI + ferrostatin1) (n = 10), and SCI + DHODH Inhibitor group (SCI + teriflunomide) (n = 10). Ten rats in the sham group only received laminectomy without SCI. To induce spinal cord injury, spinal cord injury surgery was performed in the middle thoracic region of rats (T8-T9).
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Response regulation | The application of DHODH is a potential treatment for spinal cord injury (SCI). DHODH can reduce the ferroptosis of neurons after spinal cord injury by regulating the P53/ALOX15 signaling pathway, thereby alleviating spinal cord injury. | ||||
Experiment 2 Reporting the Ferroptosis Target of This Regulator | [1] | ||||
Target for Ferroptosis | Driver | ||||
Responsed Disease | Spinal cord injury | ICD-11: ND51 | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
PC12 cells | Adrenal gland pheochromocytoma | Rattus norvegicus | CVCL_0481 | |
In Vivo Model |
Forty female Sprague-Dawley rats (200-300 g, 8 weeks old) were purchased from the Animal Experiment Center of Fudan University. Forty rats were randomly divided into four groups: sham operation group (n = 10), SCI group (n = 10), SCI + ferroptosis inhibitor group (SCI + ferrostatin1) (n = 10), and SCI + DHODH Inhibitor group (SCI + teriflunomide) (n = 10). Ten rats in the sham group only received laminectomy without SCI. To induce spinal cord injury, spinal cord injury surgery was performed in the middle thoracic region of rats (T8-T9).
Click to Show/Hide
|
||||
Response regulation | The application of DHODH is a potential treatment for spinal cord injury (SCI). DHODH can reduce the ferroptosis of neurons after spinal cord injury by regulating the P53/ALOX15 signaling pathway, thereby alleviating spinal cord injury. | ||||
Polyunsaturated fatty acid lipoxygenase ALOX12 (ALOX12) [Driver]
In total 1 item(s) under this target | |||||
Experiment 1 Reporting the Ferroptosis Target of This Regulator | [2] | ||||
Target for Ferroptosis | Driver | ||||
Responsed Disease | Anemia | ICD-11: 3A9Z | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
AHH-1 cells | Normal | Homo sapiens | CVCL_3640 | |
In Vivo Model |
4-week male C57BL/6J mice (20-22 g) were obtained from the vital river and preconditioned for one week. Mice were divided into two groups, either exposed to benzene or fresh air in the exposure system for 6 h/day, 6 days/week, for two months. In the last exposure day, the mice were fast for 10 h. Subsequently, the mice were injected with tribromoethanol (T48402, Sigma, USA) (300 mg/kg).
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Response regulation | The iron-regulatory system IRP1, ferroptosis regulator DHODH, and fatty acids metabolism rate-limiting enzyme ALOX12 were the crucial influencers in regulating ferroptosis, this provides the potential target in attenuating benzene-induced anemia of inflammation. | ||||
Phospholipid hydroperoxide glutathione peroxidase (GPX4) [Suppressor]
In total 1 item(s) under this target | |||||
Experiment 1 Reporting the Ferroptosis Target of This Regulator | [3] | ||||
Target for Ferroptosis | Suppressor | ||||
Responsed Disease | Hereditary Leiomyomatosis | ICD-11: 2C90 | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
UM-RC-2 cells | Clear cell renal carcinoma | Homo sapiens | CVCL_2739 | |
UM-RC-6 cells | Renal cell carcinoma | Homo sapiens | CVCL_2741 | ||
RCC4 cells | Clear cell renal cell carcinoma | Homo sapiens | CVCL_0498 | ||
TK-10 cells | Renal carcinoma | Homo sapiens | CVCL_1773 | ||
HT-1080 cells | Fibrosarcoma | Homo sapiens | CVCL_0317 | ||
NCI-H226 cells | Pleural epithelioid mesothelioma | Homo sapiens | CVCL_1544 | ||
In Vivo Model |
5 x 106 HT-1080 or 1 x 107 NCI-H226 cells were injected into mice subcutaneously. When the tumor reached 50-100 mm3, the mice were assigned randomly into different treatment groups. Brequinar or sulfasalazine was dissolved in dimethyl sulfoxide (DMSO) and diluted in PBS. Brequinar was intraperitoneally injected into mice at a dose of 30 mg/kg every three days. Sulfasalazine was intraperitoneally injected daily at a dose of 100 mg/kg. Liproxstatin-1 diluted in PBS was intraperitoneally injected daily at a dose of 10 mg/kg. The daily injection of brequinar, sulfasalazine, or liproxstatin-1 was continued until the endpoint as indicated in the corresponding figures.
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Response regulation | DHODH operates in parallel to mitochondrial GPX4 (but independently of cytosolic GPX4 or FSP1) to inhibit ferroptosis in the mitochondrial inner membrane by reducing ubiquinone to ubiquinol (a radical-trapping antioxidant with anti-ferroptosis activity) in Clear cell renal carcinoma. | ||||
Hereditary Leiomyomatosis [ICD-11: 2C90]
In total 1 item(s) under this disease | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [3] | ||||
Target Regulator | Dihydroorotate dehydrogenase (quinone), mitochondrial (DHODH) | Protein coding | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
UM-RC-2 cells | Clear cell renal carcinoma | Homo sapiens | CVCL_2739 | |
UM-RC-6 cells | Renal cell carcinoma | Homo sapiens | CVCL_2741 | ||
RCC4 cells | Clear cell renal cell carcinoma | Homo sapiens | CVCL_0498 | ||
TK-10 cells | Renal carcinoma | Homo sapiens | CVCL_1773 | ||
HT-1080 cells | Fibrosarcoma | Homo sapiens | CVCL_0317 | ||
NCI-H226 cells | Pleural epithelioid mesothelioma | Homo sapiens | CVCL_1544 | ||
In Vivo Model |
5 x 106 HT-1080 or 1 x 107 NCI-H226 cells were injected into mice subcutaneously. When the tumor reached 50-100 mm3, the mice were assigned randomly into different treatment groups. Brequinar or sulfasalazine was dissolved in dimethyl sulfoxide (DMSO) and diluted in PBS. Brequinar was intraperitoneally injected into mice at a dose of 30 mg/kg every three days. Sulfasalazine was intraperitoneally injected daily at a dose of 100 mg/kg. Liproxstatin-1 diluted in PBS was intraperitoneally injected daily at a dose of 10 mg/kg. The daily injection of brequinar, sulfasalazine, or liproxstatin-1 was continued until the endpoint as indicated in the corresponding figures.
Click to Show/Hide
|
||||
Response regulation | DHODH operates in parallel to mitochondrial GPX4 (but independently of cytosolic GPX4 or FSP1) to inhibit ferroptosis in the mitochondrial inner membrane by reducing ubiquinone to ubiquinol (a radical-trapping antioxidant with anti-ferroptosis activity) in Clear cell renal carcinoma. | ||||
Anemia [ICD-11: 3A9Z]
In total 1 item(s) under this disease | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [2] | ||||
Target Regulator | Dihydroorotate dehydrogenase (quinone), mitochondrial (DHODH) | Protein coding | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
AHH-1 cells | Normal | Homo sapiens | CVCL_3640 | |
In Vivo Model |
4-week male C57BL/6J mice (20-22 g) were obtained from the vital river and preconditioned for one week. Mice were divided into two groups, either exposed to benzene or fresh air in the exposure system for 6 h/day, 6 days/week, for two months. In the last exposure day, the mice were fast for 10 h. Subsequently, the mice were injected with tribromoethanol (T48402, Sigma, USA) (300 mg/kg).
Click to Show/Hide
|
||||
Response regulation | The iron-regulatory system IRP1, ferroptosis regulator DHODH, and fatty acids metabolism rate-limiting enzyme ALOX12 were the crucial influencers in regulating ferroptosis, this provides the potential target in attenuating benzene-induced anemia of inflammation. | ||||
Spinal cord injury [ICD-11: ND51]
In total 2 item(s) under this disease | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
Target Regulator | Dihydroorotate dehydrogenase (quinone), mitochondrial (DHODH) | Protein coding | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
PC12 cells | Adrenal gland pheochromocytoma | Rattus norvegicus | CVCL_0481 | |
In Vivo Model |
Forty female Sprague-Dawley rats (200-300 g, 8 weeks old) were purchased from the Animal Experiment Center of Fudan University. Forty rats were randomly divided into four groups: sham operation group (n = 10), SCI group (n = 10), SCI + ferroptosis inhibitor group (SCI + ferrostatin1) (n = 10), and SCI + DHODH Inhibitor group (SCI + teriflunomide) (n = 10). Ten rats in the sham group only received laminectomy without SCI. To induce spinal cord injury, spinal cord injury surgery was performed in the middle thoracic region of rats (T8-T9).
Click to Show/Hide
|
||||
Response regulation | The application of DHODH is a potential treatment for spinal cord injury (SCI). DHODH can reduce the ferroptosis of neurons after spinal cord injury by regulating the P53/ALOX15 signaling pathway, thereby alleviating spinal cord injury. | ||||
Experiment 2 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
Target Regulator | Dihydroorotate dehydrogenase (quinone), mitochondrial (DHODH) | Protein coding | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
PC12 cells | Adrenal gland pheochromocytoma | Rattus norvegicus | CVCL_0481 | |
In Vivo Model |
Forty female Sprague-Dawley rats (200-300 g, 8 weeks old) were purchased from the Animal Experiment Center of Fudan University. Forty rats were randomly divided into four groups: sham operation group (n = 10), SCI group (n = 10), SCI + ferroptosis inhibitor group (SCI + ferrostatin1) (n = 10), and SCI + DHODH Inhibitor group (SCI + teriflunomide) (n = 10). Ten rats in the sham group only received laminectomy without SCI. To induce spinal cord injury, spinal cord injury surgery was performed in the middle thoracic region of rats (T8-T9).
Click to Show/Hide
|
||||
Response regulation | The application of DHODH is a potential treatment for spinal cord injury (SCI). DHODH can reduce the ferroptosis of neurons after spinal cord injury by regulating the P53/ALOX15 signaling pathway, thereby alleviating spinal cord injury. | ||||
References