Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG30006)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
MEG3
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).
Browse Target
Browse Disease
Unspecific Target [Unspecific Target]
| In total 1 item(s) under this target | |||||
| Experiment 1 Reporting the Ferroptosis Target of This Regulator | [1] | ||||
| Responsed Disease | Cerebral ischaemic stroke | ICD-11: 8B11 | |||
| Pathway Response | Ferroptosis | hsa04216 | |||
| Fatty acid metabolism | hsa01212 | ||||
| Apoptosis | hsa04210 | ||||
| Cell Process | Cell ferroptosis | ||||
| Cell apoptosis | |||||
In Vitro Model |
rRBMECs (Rat brain microvascular endothelial cells) | ||||
| In Vivo Model |
Sprague Dawley (SD) rats (n = 60) aged three weeks were purchased from the Experimental Animal Center of Xiangya Hospital of Central South University. All rats were bred in a specific pathogen-free environment in 12-h lightdark cycle and fed with rodent diet and water. All rats were anaesthetized with inhaling isoflurane (2%, CAS NO. 64181101, Lunan Pharmaceutical Co., LTD. Shandong, China) and sacrificed by cervical dislocation. The whole brain was removed after opening the cranial cavity.
Click to Show/Hide
|
||||
| Response regulation | OGD combined with hyperglycemic reperfusion promoted Meg3 expression and there was positive correlation between Meg3 and p53 expression in RBMVECs. Subsequently, p53 inhibited the activity of GPX4 by binding with its promoter. The Meg3-p53 signaling pathway mediated the ferroptosis of RBMVECs upon injury induced by OGD combined with hyperglycemic reperfusion and Meg3 has been considered as an important mediator in regulating diabetic brain ischemic injury. | ||||
Cerebral ischaemic stroke [ICD-11: 8B11]
| In total 1 item(s) under this disease | |||||
| Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
| Target Regulator | MEG3 (IncRNA) | lncRNA | |||
| Pathway Response | Ferroptosis | hsa04216 | |||
| Fatty acid metabolism | hsa01212 | ||||
| Apoptosis | hsa04210 | ||||
| Cell Process | Cell ferroptosis | ||||
| Cell apoptosis | |||||
In Vitro Model |
rRBMECs (Rat brain microvascular endothelial cells) | ||||
| In Vivo Model |
Sprague Dawley (SD) rats (n = 60) aged three weeks were purchased from the Experimental Animal Center of Xiangya Hospital of Central South University. All rats were bred in a specific pathogen-free environment in 12-h lightdark cycle and fed with rodent diet and water. All rats were anaesthetized with inhaling isoflurane (2%, CAS NO. 64181101, Lunan Pharmaceutical Co., LTD. Shandong, China) and sacrificed by cervical dislocation. The whole brain was removed after opening the cranial cavity.
Click to Show/Hide
|
||||
| Response regulation | OGD combined with hyperglycemic reperfusion promoted Meg3 expression and there was positive correlation between Meg3 and p53 expression in RBMVECs. Subsequently, p53 inhibited the activity of GPX4 by binding with its promoter. The Meg3-p53 signaling pathway mediated the ferroptosis of RBMVECs upon injury induced by OGD combined with hyperglycemic reperfusion and Meg3 has been considered as an important mediator in regulating diabetic brain ischemic injury. | ||||