Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG10097)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
ENO3
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 | Marker/Suppressor | ||||
Responsed Disease | Nonalcoholic fatty liver disease | ICD-11: DB92 | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
L-02 cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_6926 | |
In Vivo Model |
Eight-week-old C57BL/6 mice, body weight about 22-24 g, male (n = 24) were purchased from Beijing Vital River Laboratory Animal Technology Co. Ltd China. The mice were randomly divided into four groups and were maintained on a MCD diet (Medicience, Yangzhou, China) for 4, 8, and 12 weeks to induce NASH. Liver tissue and blood samples (from the eyeballs of the mice) were harvested for further analyses. Mice on a normal diet were used as the control.
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Response regulation | ENO3 promoted the progression of NASH by negatively regulating ferroptosis via elevating GPX4 expression and lipid accumulation. These findings provided solid foundation for the mechanism of ferroptosis on the progression of NASH regulated by ENO3, suggesting that ENO3 may be a potential therapeutic target for non-alcoholic fatty liver disease. | ||||
Nonalcoholic fatty liver disease [ICD-11: DB92]
In total 1 item(s) under this disease | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
Target Regulator | Beta-enolase (ENO3) | Protein coding | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
L-02 cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_6926 | |
In Vivo Model |
Eight-week-old C57BL/6 mice, body weight about 22-24 g, male (n = 24) were purchased from Beijing Vital River Laboratory Animal Technology Co. Ltd China. The mice were randomly divided into four groups and were maintained on a MCD diet (Medicience, Yangzhou, China) for 4, 8, and 12 weeks to induce NASH. Liver tissue and blood samples (from the eyeballs of the mice) were harvested for further analyses. Mice on a normal diet were used as the control.
Click to Show/Hide
|
||||
Response regulation | ENO3 promoted the progression of NASH by negatively regulating ferroptosis via elevating GPX4 expression and lipid accumulation. These findings provided solid foundation for the mechanism of ferroptosis on the progression of NASH regulated by ENO3, suggesting that ENO3 may be a potential therapeutic target for non-alcoholic fatty liver disease. | ||||