Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG20084)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
mmu-miR-351-5p
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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Polyunsaturated fatty acid 5-lipoxygenase (ALOX5) [Driver]
| In total 1 item(s) under this target | |||||
| Experiment 1 Reporting the Ferroptosis Target of This Regulator | [1] | ||||
| Target for Ferroptosis | Driver | ||||
| Responsed Disease | Traumatic brain injury | ICD-11: NA07 | |||
| Responsed Drug | Melatonin | Investigative | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Ferroptosis | hsa04216 | ||||
| Cell Process | Cell ferroptosis | ||||
In Vitro Model |
bEnd.3 cells | Normal | Mus musculus | CVCL_0170 | |
| In Vivo Model |
Male C57BL/6 mice aged 6-8 weeks were purchased from the Chongqing Medical University Animal Experiment Center (Chongqing, China). Mice were randomly allocated into three groups including sham group, TBI group, and melatonin treatment group. 30 mice were used for MRI and cerebral blood flow (CBF) monitoring at the 3rd and 7th day, with 5 in each group; 15 mice were used for EEG detection at the 14th and 30th days, training and testing inwater mazeduring the 25th-30th days, with 5 in each group. 15 mice were used for brain water content determination on the 3rd day, with 5 in each group. 9 mice were used for RNA sequencing, with 3 in each group; 75 mice were used for brain tissue acquisition, with 5 in each group with 5 time points (1st, 3rd, 7th, 14th, and 30th day after the operation).
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| Response regulation | Melatonin administration reduced the level of circPtpn14 (mmu_circ_0000130), which functioned by acting as a miR-351-5p sponge to positively regulate the expression of the ferroptosis-related 5-lipoxygenase (5-LOX). In addition, melatonin alleviated longterm sleep disorders and improved neurological function in Traumatic brain injury (TBI) mice. Thus, these findings suggested that melatonin might potentially protect the injured brain by attenuating ferroptosis and ER stress. | ||||
Traumatic brain injury [ICD-11: NA07]
| In total 1 item(s) under this disease | |||||
| Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
| Target Regulator | mmu-miR-351-5p (miRNA) | miRNA | |||
| Responsed Drug | Melatonin | Investigative | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Ferroptosis | hsa04216 | ||||
| Cell Process | Cell ferroptosis | ||||
In Vitro Model |
bEnd.3 cells | Normal | Mus musculus | CVCL_0170 | |
| In Vivo Model |
Male C57BL/6 mice aged 6-8 weeks were purchased from the Chongqing Medical University Animal Experiment Center (Chongqing, China). Mice were randomly allocated into three groups including sham group, TBI group, and melatonin treatment group. 30 mice were used for MRI and cerebral blood flow (CBF) monitoring at the 3rd and 7th day, with 5 in each group; 15 mice were used for EEG detection at the 14th and 30th days, training and testing inwater mazeduring the 25th-30th days, with 5 in each group. 15 mice were used for brain water content determination on the 3rd day, with 5 in each group. 9 mice were used for RNA sequencing, with 3 in each group; 75 mice were used for brain tissue acquisition, with 5 in each group with 5 time points (1st, 3rd, 7th, 14th, and 30th day after the operation).
Click to Show/Hide
|
||||
| Response regulation | Melatonin administration reduced the level of circPtpn14 (mmu_circ_0000130), which functioned by acting as a miR-351-5p sponge to positively regulate the expression of the ferroptosis-related 5-lipoxygenase (5-LOX). In addition, melatonin alleviated longterm sleep disorders and improved neurological function in Traumatic brain injury (TBI) mice. Thus, these findings suggested that melatonin might potentially protect the injured brain by attenuating ferroptosis and ER stress. | ||||
Melatonin
[Investigative]
| In total 1 item(s) under this drug | |||||
| Experiment 1 Reporting the Ferroptosis-centered Drug Response | [1] | ||||
| Drug for Ferroptosis | Suppressor | ||||
| Response Target | Polyunsaturated fatty acid 5-lipoxygenase (ALOX5) | Driver | |||
| Responsed Disease | Traumatic brain injury | ICD-11: NA07 | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Ferroptosis | hsa04216 | ||||
| Cell Process | Cell ferroptosis | ||||
In Vitro Model |
bEnd.3 cells | Normal | Mus musculus | CVCL_0170 | |
| In Vivo Model |
Male C57BL/6 mice aged 6-8 weeks were purchased from the Chongqing Medical University Animal Experiment Center (Chongqing, China). Mice were randomly allocated into three groups including sham group, TBI group, and melatonin treatment group. 30 mice were used for MRI and cerebral blood flow (CBF) monitoring at the 3rd and 7th day, with 5 in each group; 15 mice were used for EEG detection at the 14th and 30th days, training and testing inwater mazeduring the 25th-30th days, with 5 in each group. 15 mice were used for brain water content determination on the 3rd day, with 5 in each group. 9 mice were used for RNA sequencing, with 3 in each group; 75 mice were used for brain tissue acquisition, with 5 in each group with 5 time points (1st, 3rd, 7th, 14th, and 30th day after the operation).
Click to Show/Hide
|
||||
| Response regulation | Melatonin administration reduced the level of circPtpn14 (mmu_circ_0000130), which functioned by acting as a miR-351-5p sponge to positively regulate the expression of the ferroptosis-related 5-lipoxygenase (5-LOX). In addition, melatonin alleviated longterm sleep disorders and improved neurological function in Traumatic brain injury (TBI) mice. Thus, these findings suggested that melatonin might potentially protect the injured brain by attenuating ferroptosis and ER stress. | ||||