Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG20030)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
hsa-miR-190a-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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Glutaminase liver isoform, mitochondrial (GLS2) [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 | Acute myocardial infarction | ICD-11: BA41 | ||
| Pathway Response | Glutathione metabolism | hsa00480 | ||
| Ferroptosis | hsa04216 | |||
| Cell Process | Cell ferroptosis | |||
| Cell proliferation | ||||
In Vitro Model |
CHO-S/H9C2 cells | Normal | Cricetulus griseus | CVCL_A0TS |
| HEK-293T cells | Normal | Homo sapiens | CVCL_0063 | |
| Response regulation | MiR-190a-5p negatively regulate ferroptosis via directly targeting GLS2 in rat cardiomyocyte H9c2 cells. Forced expression of miR-190a-5p inhibited GLS2, resulting in downregulation of ROS, MDA and Fe2+accumulation. In summary, miR-190a-5p plays an essential role in regulation of ferroptosis of cardiomyocytes and suggest a potential therapeutic target for myocardial infarction. | |||
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 | hsa-miR-190a-5p (miRNA) | miRNA | ||
| Pathway Response | Glutathione metabolism | hsa00480 | ||
| Ferroptosis | hsa04216 | |||
| Cell Process | Cell ferroptosis | |||
| Cell proliferation | ||||
In Vitro Model |
CHO-S/H9C2 cells | Normal | Cricetulus griseus | CVCL_A0TS |
| HEK-293T cells | Normal | Homo sapiens | CVCL_0063 | |
| Response regulation | MiR-190a-5p negatively regulate ferroptosis via directly targeting GLS2 in rat cardiomyocyte H9c2 cells. Forced expression of miR-190a-5p inhibited GLS2, resulting in downregulation of ROS, MDA and Fe2+accumulation. In summary, miR-190a-5p plays an essential role in regulation of ferroptosis of cardiomyocytes and suggest a potential therapeutic target for myocardial infarction. | |||
