Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG10021)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
SMAD7
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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Unspecific Target [Unspecific Target]
| In total 1 item(s) under this target | |||||
| Experiment 1 Reporting the Ferroptosis Target of This Regulator | [1] | ||||
| Responsed Disease | Cardiomyopathy | ICD-11: BC43 | |||
| Responsed Drug | Atorvastatin | Investigative | |||
| Pathway Response | Ferroptosis | hsa04216 | |||
| Cell Process | Cell ferroptosis | ||||
In Vitro Model |
CHO-S/H9C2 cells | Normal | Cricetulus griseus | CVCL_A0TS | |
| In Vivo Model |
A total of 18 Wistar rats (250~300 g) were purchased from Hunan slake Jingda experimental animal Co., Ltd. The rats were randomly divided into the Sham group, I/R group, and I/R + ATV group (n = 6/group).They received standard diet and water before myocardial I/R. Rats in the I/R + ATV group were orally treated with ATV (10 mg/kg/d) for 2 weeks before myocardial I/R (9).The Sham and I/R model rats were constructed as follows: The rats were anesthetized with sodium pentobarbital (50 mg/kg, intraperitoneal injection), ligation of the left anterior descending branch with 4-0 silk thread for 30 min, and then reperfusion for 180 min. In the sham control group, the entire procedure was performed with silk thread passing below the coronary artery, but the LAD coronary artery was not ligated. At the end of reperfusion, the rats were given excessive isoflurane for 10 min and sacrificed by bloodletting. Then the rat myocardial tissues were isolated for subsequent detection.
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| Response regulation | Atorvastatin intervention blocked erastin or H/R-induced ferroptosis in H9C2 cells by activating SMAD7 expression and thereby down-regulating the hepcidin/FPN1 pathway. The in vivo study also demonstrated that ATV inhibited ferroptosis in ischemia-reperfusion cardiomyopathy rat myocardium through the SMAD7/hepcidin pathway. | ||||
Cardiomyopathy [ICD-11: BC43]
| In total 1 item(s) under this disease | |||||
| Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
| Target Regulator | Mothers against decapentaplegic homolog 7 (SMAD7) | Protein coding | |||
| Responsed Drug | Atorvastatin | Investigative | |||
| Pathway Response | Ferroptosis | hsa04216 | |||
| Cell Process | Cell ferroptosis | ||||
In Vitro Model |
CHO-S/H9C2 cells | Normal | Cricetulus griseus | CVCL_A0TS | |
| In Vivo Model |
A total of 18 Wistar rats (250~300 g) were purchased from Hunan slake Jingda experimental animal Co., Ltd. The rats were randomly divided into the Sham group, I/R group, and I/R + ATV group (n = 6/group).They received standard diet and water before myocardial I/R. Rats in the I/R + ATV group were orally treated with ATV (10 mg/kg/d) for 2 weeks before myocardial I/R (9).The Sham and I/R model rats were constructed as follows: The rats were anesthetized with sodium pentobarbital (50 mg/kg, intraperitoneal injection), ligation of the left anterior descending branch with 4-0 silk thread for 30 min, and then reperfusion for 180 min. In the sham control group, the entire procedure was performed with silk thread passing below the coronary artery, but the LAD coronary artery was not ligated. At the end of reperfusion, the rats were given excessive isoflurane for 10 min and sacrificed by bloodletting. Then the rat myocardial tissues were isolated for subsequent detection.
Click to Show/Hide
|
||||
| Response regulation | Atorvastatin intervention blocked erastin or H/R-induced ferroptosis in H9C2 cells by activating SMAD7 expression and thereby down-regulating the hepcidin/FPN1 pathway. The in vivo study also demonstrated that ATV inhibited ferroptosis in ischemia-reperfusion cardiomyopathy rat myocardium through the SMAD7/hepcidin pathway. | ||||
Atorvastatin
[Investigative]
| In total 1 item(s) under this drug | |||||
| Experiment 1 Reporting the Ferroptosis-centered Drug Response | [1] | ||||
| Drug for Ferroptosis | Suppressor | ||||
| Response Target | Unspecific Target | ||||
| Responsed Disease | Cardiomyopathy | ICD-11: BC43 | |||
| Pathway Response | Ferroptosis | hsa04216 | |||
| Cell Process | Cell ferroptosis | ||||
In Vitro Model |
CHO-S/H9C2 cells | Normal | Cricetulus griseus | CVCL_A0TS | |
| In Vivo Model |
A total of 18 Wistar rats (250~300 g) were purchased from Hunan slake Jingda experimental animal Co., Ltd. The rats were randomly divided into the Sham group, I/R group, and I/R + ATV group (n = 6/group).They received standard diet and water before myocardial I/R. Rats in the I/R + ATV group were orally treated with ATV (10 mg/kg/d) for 2 weeks before myocardial I/R (9).The Sham and I/R model rats were constructed as follows: The rats were anesthetized with sodium pentobarbital (50 mg/kg, intraperitoneal injection), ligation of the left anterior descending branch with 4-0 silk thread for 30 min, and then reperfusion for 180 min. In the sham control group, the entire procedure was performed with silk thread passing below the coronary artery, but the LAD coronary artery was not ligated. At the end of reperfusion, the rats were given excessive isoflurane for 10 min and sacrificed by bloodletting. Then the rat myocardial tissues were isolated for subsequent detection.
Click to Show/Hide
|
||||
| Response regulation | Atorvastatin intervention blocked erastin or H/R-induced ferroptosis in H9C2 cells by activating SMAD7 expression and thereby down-regulating the hepcidin/FPN1 pathway. The in vivo study also demonstrated that ATV inhibited ferroptosis in ischemia-reperfusion cardiomyopathy rat myocardium through the SMAD7/hepcidin pathway. | ||||