Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG10505)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
SOD2
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 | LCZ696 | Approved | |||
Pathway Response | Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
CHO-S/H9C2 cells | Normal | Cricetulus griseus | CVCL_A0TS | |
In Vivo Model |
All animal protocols were approved by the Animal Care and Use Committee of TaizhouHospital, affiliated to Zhejiang University (Taizhou, China). Twenty-four 2-month-old male Wistar rats weighing 190-220 g were purchased from the Experimental Animal Center of Basi Medicine, Zhejiang Chinese Medical University. The animals were reared under a 12 h light/12 h dark cycle at a relative humidity of 55 ± 5% and temperature of 23 ± 2 , with unrestricted access to food and water. All animals were acclimatized to laboratory conditions for 1 week before the experiments and were randomly divided into four groups: control group (CG, n = 6); LCZ696 group (LCZ, n = 6); DOX group (DOX, n = 6); and DOX + LCZ696 group (DOX + LCZ, n = 6). The CG received saline solution by gavage for 6 weeks (2 mL/day), while the treatment groups received DOX (Cat. HY-15142A, MedChemExpress, USA), LCZ696 (Cat. HY-18204A, MedChemExpress, USA), or DOX + LCZ696. DOX was administered at a dose of 2.5 mg/kg once a week for 6 weeks via tailvein injection. LCZ696 (60 mg/kg/day) was administered by gavage for 6 weeks. Body weight was measured weekly.
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Response regulation | LCZ696 treatment increased SIRT3 expression and deacetylated its target gene SOD2, and these changes were mediated by AKT activation. Collectively, LCZ696 prevents DOX-induced cardiotoxicity by inhibiting ferroptosis via AKT/SIRT3/SOD2 signaling pathway activation. | ||||
Cardiomyopathy [ICD-11: BC43]
In total 1 item(s) under this disease | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
Target Regulator | Superoxide dismutase [Mn], mitochondrial (SOD2) | Protein coding | |||
Responsed Drug | LCZ696 | Approved | |||
Pathway Response | Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
CHO-S/H9C2 cells | Normal | Cricetulus griseus | CVCL_A0TS | |
In Vivo Model |
All animal protocols were approved by the Animal Care and Use Committee of TaizhouHospital, affiliated to Zhejiang University (Taizhou, China). Twenty-four 2-month-old male Wistar rats weighing 190-220 g were purchased from the Experimental Animal Center of Basi Medicine, Zhejiang Chinese Medical University. The animals were reared under a 12 h light/12 h dark cycle at a relative humidity of 55 ± 5% and temperature of 23 ± 2 , with unrestricted access to food and water. All animals were acclimatized to laboratory conditions for 1 week before the experiments and were randomly divided into four groups: control group (CG, n = 6); LCZ696 group (LCZ, n = 6); DOX group (DOX, n = 6); and DOX + LCZ696 group (DOX + LCZ, n = 6). The CG received saline solution by gavage for 6 weeks (2 mL/day), while the treatment groups received DOX (Cat. HY-15142A, MedChemExpress, USA), LCZ696 (Cat. HY-18204A, MedChemExpress, USA), or DOX + LCZ696. DOX was administered at a dose of 2.5 mg/kg once a week for 6 weeks via tailvein injection. LCZ696 (60 mg/kg/day) was administered by gavage for 6 weeks. Body weight was measured weekly.
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|
||||
Response regulation | LCZ696 treatment increased SIRT3 expression and deacetylated its target gene SOD2, and these changes were mediated by AKT activation. Collectively, LCZ696 prevents DOX-induced cardiotoxicity by inhibiting ferroptosis via AKT/SIRT3/SOD2 signaling pathway activation. | ||||
LCZ696
[Approved]
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 |
All animal protocols were approved by the Animal Care and Use Committee of TaizhouHospital, affiliated to Zhejiang University (Taizhou, China). Twenty-four 2-month-old male Wistar rats weighing 190-220 g were purchased from the Experimental Animal Center of Basi Medicine, Zhejiang Chinese Medical University. The animals were reared under a 12 h light/12 h dark cycle at a relative humidity of 55 ± 5% and temperature of 23 ± 2 , with unrestricted access to food and water. All animals were acclimatized to laboratory conditions for 1 week before the experiments and were randomly divided into four groups: control group (CG, n = 6); LCZ696 group (LCZ, n = 6); DOX group (DOX, n = 6); and DOX + LCZ696 group (DOX + LCZ, n = 6). The CG received saline solution by gavage for 6 weeks (2 mL/day), while the treatment groups received DOX (Cat. HY-15142A, MedChemExpress, USA), LCZ696 (Cat. HY-18204A, MedChemExpress, USA), or DOX + LCZ696. DOX was administered at a dose of 2.5 mg/kg once a week for 6 weeks via tailvein injection. LCZ696 (60 mg/kg/day) was administered by gavage for 6 weeks. Body weight was measured weekly.
Click to Show/Hide
|
||||
Response regulation | LCZ696 treatment increased SIRT3 expression and deacetylated its target gene SOD2, and these changes were mediated by AKT activation. Collectively, LCZ696 prevents DOX-induced cardiotoxicity by inhibiting ferroptosis via AKT/SIRT3/SOD2 signaling pathway activation. | ||||