Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG20112)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
hsa-miR-224-5p
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).
Browse Target
Browse Disease
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 | Congestive heart failure | ICD-11: BD10 | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Ferroptosis | hsa04216 | ||||
| Cell Process | Cell ferroptosis | ||||
In Vitro Model |
mMTs (Mouse myocardial tissues) | ||||
| In Vivo Model |
Six-week-old male C57/BL6J mice (weighting ~18-20 g) were supplied by the Shenyang Military Region General Hospital Experimental Animal Center. The mice were fed a standard diet and had unlimited access to drinking water. After 2 weeks of feeding, the mice were randomly assigned to TAC group (n = 15) and SHAM group (n = 16), and then anesthetized by intraperitoneal injection of 50 mg/kg pentobarbital sodium. To allow direct access to the transverse aorta, the mice a horizontal incision (5 mm in length) was made at the suprasternal notch. TAC operation was then performed by ligating the aorta between the right innominate and left carotid arteries using a 27G needle tied with 7-0 silk suture. The needle was promptly withdrawn, leaving the aortic constriction in place. The surgical procedure of mice in SHAM group was similar to that of mice in TAC group, except that the 7-0 silk suture was only crossed through the aortic arch without ligation.
Click to Show/Hide
|
||||
| Response regulation | MiR-224-5p was indeed the downstream target of circSnx12, and miR-224-5p could bind to the 3'-UTR region of FTH1 and regulate its expression level. Therefore, it is speculated that low circSnx12 expression and high miR-224-5p expression can downregulate FTH1 expression, directly regulate iron overload in myocardial cells, and ultimately leads to cardiac cell death. This new approach reveals potential circRNA targets for the treatment of heart failure. | ||||
Congestive heart failure [ICD-11: BD10]
| In total 1 item(s) under this disease | |||||
| Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
| Target Regulator | hsa-miR-224-5p (miRNA) | miRNA | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Ferroptosis | hsa04216 | ||||
| Cell Process | Cell ferroptosis | ||||
In Vitro Model |
mMTs (Mouse myocardial tissues) | ||||
| In Vivo Model |
Six-week-old male C57/BL6J mice (weighting ~18-20 g) were supplied by the Shenyang Military Region General Hospital Experimental Animal Center. The mice were fed a standard diet and had unlimited access to drinking water. After 2 weeks of feeding, the mice were randomly assigned to TAC group (n = 15) and SHAM group (n = 16), and then anesthetized by intraperitoneal injection of 50 mg/kg pentobarbital sodium. To allow direct access to the transverse aorta, the mice a horizontal incision (5 mm in length) was made at the suprasternal notch. TAC operation was then performed by ligating the aorta between the right innominate and left carotid arteries using a 27G needle tied with 7-0 silk suture. The needle was promptly withdrawn, leaving the aortic constriction in place. The surgical procedure of mice in SHAM group was similar to that of mice in TAC group, except that the 7-0 silk suture was only crossed through the aortic arch without ligation.
Click to Show/Hide
|
||||
| Response regulation | MiR-224-5p was indeed the downstream target of circSnx12, and miR-224-5p could bind to the 3'-UTR region of FTH1 and regulate its expression level. Therefore, it is speculated that low circSnx12 expression and high miR-224-5p expression can downregulate FTH1 expression, directly regulate iron overload in myocardial cells, and ultimately leads to cardiac cell death. This new approach reveals potential circRNA targets for the treatment of heart failure. | ||||