Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG20104)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
rno-miR-29a-3p
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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Transferrin receptor protein 1 (TFRC) [Driver; Suppressor; Marker]
| In total 1 item(s) under this target | |||||
| Experiment 1 Reporting the Ferroptosis Target of This Regulator | [1] | ||||
| Target for Ferroptosis | Marker/Suppressor/Driver | ||||
| Responsed Disease | Ischemia/reperfusion injury | ICD-11: DB98 | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Ferroptosis | hsa04216 | ||||
| Cell Process | Cell ferroptosis | ||||
In Vitro Model |
rBMMSCs (Rat bone marrow mesenchymal stem cells) | ||||
| IAR 20 cells | Normal | Homo sapiens | CVCL_5296 | ||
| In Vivo Model |
Clean-grade male Sprague-Dawley (SD) rats were purchased from China Food and Drug Administration (Beijing, China). SD rats were fed a high-fat diet (Composition: 15% triglyceride, 15% sucrose, 10% egg yolk powder, 1% cholesterol, 0.2% bile salt, 58.8% basic feed) for 20 weeks. Hematoxylin and eosin (HE) and oil red O staining showed that the area of mixed macrovesicular steatosis was more than 60% under the microscope, indicating that a model of severe steatotic liver was established successfully. A 70% liver thermal ischemia model was established, continuously blocked for 80 min, and then, the ischemic liver was obtained 24 h after reperfusion.
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| Response regulation | miR-29a-3p, which targets IREB2, is abundant in HO-1/BMMSC-exosomes and could decrease the IREB2 protein level. The reduced IREB2 level led to an increase in the level of FTH1 and decreased the level of TFR1 through posttranscriptional regulation, which ultimately reduced the level of intracellular Fe2+ and the production of lipid ROS and inhibited the occurrence of ferroptosis in SHP-HR. In conclusion, ferroptosis plays an important role in HO-1/BMMSC-mediated alleviation of steatotic hepatic ischemia-reperfusion injury. | ||||
Iron-responsive element-binding protein 2 (IREB2) [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 | Ischemia/reperfusion injury | ICD-11: DB98 | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Ferroptosis | hsa04216 | ||||
| Cell Process | Cell ferroptosis | ||||
In Vitro Model |
rBMMSCs (Rat bone marrow mesenchymal stem cells) | ||||
| IAR 20 cells | Normal | Homo sapiens | CVCL_5296 | ||
| In Vivo Model |
Clean-grade male Sprague-Dawley (SD) rats were purchased from China Food and Drug Administration (Beijing, China). SD rats were fed a high-fat diet (Composition: 15% triglyceride, 15% sucrose, 10% egg yolk powder, 1% cholesterol, 0.2% bile salt, 58.8% basic feed) for 20 weeks. Hematoxylin and eosin (HE) and oil red O staining showed that the area of mixed macrovesicular steatosis was more than 60% under the microscope, indicating that a model of severe steatotic liver was established successfully. A 70% liver thermal ischemia model was established, continuously blocked for 80 min, and then, the ischemic liver was obtained 24 h after reperfusion.
Click to Show/Hide
|
||||
| Response regulation | miR-29a-3p, which targets IREB2, is abundant in HO-1/BMMSC-exosomes and could decrease the IREB2 protein level. The reduced IREB2 level led to an increase in the level of FTH1 and decreased the level of TFR1 through posttranscriptional regulation, which ultimately reduced the level of intracellular Fe2+ and the production of lipid ROS and inhibited the occurrence of ferroptosis in SHP-HR. In conclusion, ferroptosis plays an important role in HO-1/BMMSC-mediated alleviation of steatotic hepatic ischemia-reperfusion injury. | ||||
Ferritin heavy chain (FTH1) [Suppressor; Marker]
| 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 | Ischemia/reperfusion injury | ICD-11: DB98 | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Ferroptosis | hsa04216 | ||||
| Cell Process | Cell ferroptosis | ||||
In Vitro Model |
rBMMSCs (Rat bone marrow mesenchymal stem cells) | ||||
| IAR 20 cells | Normal | Homo sapiens | CVCL_5296 | ||
| In Vivo Model |
Clean-grade male Sprague-Dawley (SD) rats were purchased from China Food and Drug Administration (Beijing, China). SD rats were fed a high-fat diet (Composition: 15% triglyceride, 15% sucrose, 10% egg yolk powder, 1% cholesterol, 0.2% bile salt, 58.8% basic feed) for 20 weeks. Hematoxylin and eosin (HE) and oil red O staining showed that the area of mixed macrovesicular steatosis was more than 60% under the microscope, indicating that a model of severe steatotic liver was established successfully. A 70% liver thermal ischemia model was established, continuously blocked for 80 min, and then, the ischemic liver was obtained 24 h after reperfusion.
Click to Show/Hide
|
||||
| Response regulation | miR-29a-3p, which targets IREB2, is abundant in HO-1/BMMSC-exosomes and could decrease the IREB2 protein level. The reduced IREB2 level led to an increase in the level of FTH1 and decreased the level of TFR1 through posttranscriptional regulation, which ultimately reduced the level of intracellular Fe2+ and the production of lipid ROS and inhibited the occurrence of ferroptosis in SHP-HR. In conclusion, ferroptosis plays an important role in HO-1/BMMSC-mediated alleviation of steatotic hepatic ischemia-reperfusion injury. | ||||
Ischemia/reperfusion injury [ICD-11: DB98]
| In total 3 item(s) under this disease | |||||
| Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
| Target Regulator | rno-miR-29a-3p (miRNA) | miRNA | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Ferroptosis | hsa04216 | ||||
| Cell Process | Cell ferroptosis | ||||
In Vitro Model |
rBMMSCs (Rat bone marrow mesenchymal stem cells) | ||||
| IAR 20 cells | Normal | Homo sapiens | CVCL_5296 | ||
| In Vivo Model |
Clean-grade male Sprague-Dawley (SD) rats were purchased from China Food and Drug Administration (Beijing, China). SD rats were fed a high-fat diet (Composition: 15% triglyceride, 15% sucrose, 10% egg yolk powder, 1% cholesterol, 0.2% bile salt, 58.8% basic feed) for 20 weeks. Hematoxylin and eosin (HE) and oil red O staining showed that the area of mixed macrovesicular steatosis was more than 60% under the microscope, indicating that a model of severe steatotic liver was established successfully. A 70% liver thermal ischemia model was established, continuously blocked for 80 min, and then, the ischemic liver was obtained 24 h after reperfusion.
Click to Show/Hide
|
||||
| Response regulation | miR-29a-3p, which targets IREB2, is abundant in HO-1/BMMSC-exosomes and could decrease the IREB2 protein level. The reduced IREB2 level led to an increase in the level of FTH1 and decreased the level of TFR1 through posttranscriptional regulation, which ultimately reduced the level of intracellular Fe2+ and the production of lipid ROS and inhibited the occurrence of ferroptosis in SHP-HR. In conclusion, ferroptosis plays an important role in HO-1/BMMSC-mediated alleviation of steatotic hepatic ischemia-reperfusion injury. | ||||
| Experiment 2 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
| Target Regulator | rno-miR-29a-3p (miRNA) | miRNA | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Ferroptosis | hsa04216 | ||||
| Cell Process | Cell ferroptosis | ||||
In Vitro Model |
rBMMSCs (Rat bone marrow mesenchymal stem cells) | ||||
| IAR 20 cells | Normal | Homo sapiens | CVCL_5296 | ||
| In Vivo Model |
Clean-grade male Sprague-Dawley (SD) rats were purchased from China Food and Drug Administration (Beijing, China). SD rats were fed a high-fat diet (Composition: 15% triglyceride, 15% sucrose, 10% egg yolk powder, 1% cholesterol, 0.2% bile salt, 58.8% basic feed) for 20 weeks. Hematoxylin and eosin (HE) and oil red O staining showed that the area of mixed macrovesicular steatosis was more than 60% under the microscope, indicating that a model of severe steatotic liver was established successfully. A 70% liver thermal ischemia model was established, continuously blocked for 80 min, and then, the ischemic liver was obtained 24 h after reperfusion.
Click to Show/Hide
|
||||
| Response regulation | miR-29a-3p, which targets IREB2, is abundant in HO-1/BMMSC-exosomes and could decrease the IREB2 protein level. The reduced IREB2 level led to an increase in the level of FTH1 and decreased the level of TFR1 through posttranscriptional regulation, which ultimately reduced the level of intracellular Fe2+ and the production of lipid ROS and inhibited the occurrence of ferroptosis in SHP-HR. In conclusion, ferroptosis plays an important role in HO-1/BMMSC-mediated alleviation of steatotic hepatic ischemia-reperfusion injury. | ||||
| Experiment 3 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
| Target Regulator | rno-miR-29a-3p (miRNA) | miRNA | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Ferroptosis | hsa04216 | ||||
| Cell Process | Cell ferroptosis | ||||
In Vitro Model |
rBMMSCs (Rat bone marrow mesenchymal stem cells) | ||||
| IAR 20 cells | Normal | Homo sapiens | CVCL_5296 | ||
| In Vivo Model |
Clean-grade male Sprague-Dawley (SD) rats were purchased from China Food and Drug Administration (Beijing, China). SD rats were fed a high-fat diet (Composition: 15% triglyceride, 15% sucrose, 10% egg yolk powder, 1% cholesterol, 0.2% bile salt, 58.8% basic feed) for 20 weeks. Hematoxylin and eosin (HE) and oil red O staining showed that the area of mixed macrovesicular steatosis was more than 60% under the microscope, indicating that a model of severe steatotic liver was established successfully. A 70% liver thermal ischemia model was established, continuously blocked for 80 min, and then, the ischemic liver was obtained 24 h after reperfusion.
Click to Show/Hide
|
||||
| Response regulation | miR-29a-3p, which targets IREB2, is abundant in HO-1/BMMSC-exosomes and could decrease the IREB2 protein level. The reduced IREB2 level led to an increase in the level of FTH1 and decreased the level of TFR1 through posttranscriptional regulation, which ultimately reduced the level of intracellular Fe2+ and the production of lipid ROS and inhibited the occurrence of ferroptosis in SHP-HR. In conclusion, ferroptosis plays an important role in HO-1/BMMSC-mediated alleviation of steatotic hepatic ischemia-reperfusion injury. | ||||
References